eMedicine Specialties > Otolaryngology and Facial Plastic Surgery > Laryngology

Reflux Laryngitis

Author: Bardia Amirlak, MD, Fellow, Department of Plastic and Reconstructive Surgery, Case Western School of Medicine
Coauthor(s): Pamela A Mudd, BS, MD, Resident Physician, Department of Otolaryngology, University of Colorado Health Science Center; Reza Shaker, MD, Chief, Professor, Department of Internal Medicine, Division of Gastroenterology and Hepatology, Medical College of Wisconsin
Contributor Information and Disclosures

Updated: May 11, 2009

Introduction

Background

Since the late 1960s, gastroesophageal acid reflux has been implicated in the pathogenesis of several extraesophageal disorders, including laryngitis.1 Although the cause-effect relationship has been strengthened by more recent evidence, the body of evidence on causation, diagnosis, and treatment of these increasingly diagnosed disorders is still evolving.

Various symptoms, functional and structural abnormalities that involve the larynx, and other contiguous structures positioned proximal to the esophagus constitute the spectrum of these disorders. Patients presenting with extraesophageal reflux–related signs and symptoms may account for up to 10% of an otolaryngologist's practice.2 A large amount of gastroesophageal reflux (GERD)–associated and laryngopharyngeal reflux (LPR)–associated processes are treated primarily by otolaryngologists. This list includes the following:

  • Chronic laryngitis
  • Hoarseness
  • Globus sensation
  • Chronic cough or throat clearing
  • Dysphagia
  • Halitosis
  • Chronic rhinosinusitis
  • Laryngeal malacia
  • Laryngeal stenosis
  • Laryngeal carcinoma

Various terms such as laryngopharyngeal reflux (LPR), supraesophageal GERD, atypical GERD, and extraesophageal complications of GERD have been used to describe this group of symptoms and signs. Although addressed by various terms, these basically represent supraesophageal complications due to reflux of gastric acid content through the esophageal/pharyngeal/laryngeal/pulmonary axis. Although these symptoms were previously thought to constitute the spectrum of GERD, laryngopharyngeal reflux (LPR) is today thought to be a distinct entity and should be managed differently.3

The RSI documents the presence and degree of nine...

The RSI documents the presence and degree of nine laryngopharyngeal reflux (LPR) symptoms both before and after treatment; maximum score: 45.

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The RSI documents the presence and degree of nine...

The RSI documents the presence and degree of nine laryngopharyngeal reflux (LPR) symptoms both before and after treatment; maximum score: 45.


Failing to recognize laryngopharyngeal reflux (LPR) is dangerous, while overdiagnosis of laryngopharyngeal reflux (LPR) can lead to unnecessary costs and missed diagnosis. Inflamed laryngeal tissue affected by laryngopharyngeal reflux (LPR) is more easily damaged from intubation, has a high risk of progressing to contact granulomas, and may evolve to symptomatic subglottic stenosis.4

In a recent report, laryngopharyngeal reflux (LPR) symptoms were found to be more prevalent in patients with esophageal adenocarcinoma than were typical GERD symptoms, and they often represented the only sign of disease.5 On the other hand, increased awareness may lead to overdiagnosis of the condition because typical laryngopharyngeal reflux (LPR) symptoms are nonspecific and can occur in processes such as infection, vocal abuse, allergy, smoking, inhaled irritants, and alcohol abuse.3

Caution must also be taken to rule out serious processes that may present with similar symptoms, such as laryngeal cancer, before proceeding with conservative management.

Laryngopharyngeal reflux (LPR) is the term used in this article to discuss the pathogenesis of reflux laryngitis.

Pathophysiology

Major factors that have led clinicians to associate chronic supraesophageal disorders with reflux of gastric acid include the frequent lack of an etiology for some chronic laryngeal symptoms and findings, the recurrent or persistent nature of these disorders, and the benefit of empiric antireflux treatment as reported by multiple observational studies. However, the cause-effect relationship has been difficult to establish for several reasons, including the following:

  • GERD is a prevalent disorder, but only a small proportion of these patients have supraesophageal problems.
  • Although a significant subset of these patients may have abnormal esophageal acid exposure, in most patients, esophageal symptoms or esophagitis is absent.
  • Ascertaining whether supraesophageal disorders result from neurally mediated cough and chronic throat clearing or from direct injury from mucosal contact with substances in the refluxate has been difficult. However, most believe that the mucosa of the pharyngolarynx is not designed to handle the direct injury of acid or pepsin found in the refluxate.
  • Response to agents that inhibit gastric acid secretion has not been as clear as response for esophageal signs and symptoms of reflux disease.

Unfortunately, a direct relationship between refluxed gastric acid and most of these suspected supraesophageal complications have been difficult to conclusively establish to date. This dilemma is further complicated by the fact that patients with suspected pharyngeal and laryngeal complications of reflux disease frequently lack the characteristic features of GERD, including its symptom of heartburn, and some patients may have suspected reflux-induced supraesophageal and esophageal peptic injuries, which are independent of each other.

Two hypotheses exist about how gastric acid precipitates extraesophageal pathologic response. The first purports direct acid-pepsin injury to the larynx and surrounding tissues. The second hypothesis suggests that acid in the distal esophagus stimulates vagal-mediated reflexes that result in bronchoconstriction and chronic throat clearing and coughing, eventually leading to mucosal lesions. These 2 mechanisms may act in combination to produce the pathologic changes seen in laryngopharyngeal reflux (LPR).6

The following 4 physiological barriers protect the upper aerodigestive tract from reflux injury:

  • The lower esophageal sphincter
  • Esophageal motor function with acid clearance
  • Esophageal mucosal tissue resistance
  • The upper esophageal sphincter

The delicate ciliated epithelium of the respiratory tract is sensitive to damage when these mechanisms fail. Dysfunction in the cilia leads to mucus stasis. The accumulation of mucus produces sensations that provoke chronic throat clearing. Direct irritation of the upper airway by gastric refluxate can cause laryngospasm, producing symptoms of chronic coughing and choking.

The combination of direct injury by refluxate and symptoms such as chronic laryngospasm and throat clearing can lead to vocal cord edema, contact ulcers, and granulomas that cause other LPR-associated symptoms such as hoarseness, globus pharyngeus, and sore throat.

Evidence suggests that in both healthy and patient populations the refluxed gastric acid may come into contact with structures as high as the pharynx. Furthermore, several signs of laryngeal irritation, which are generally considered to be signs of laryngopharyngeal reflux (LPR), were found to be present in a high percentage of asymptomatic individuals on laryngoscopic examination.7

These findings suggest the existence of interindividual variability in terms of mucosal resistance to acid exposure, both in the esophagus and pharyngolarynx. Currently, the understanding of the pharyngolaryngeal defense mechanisms against refluxed acid is limited, and the natural history of the disease is unknown. This problem is further magnified by the fact that pharyngolaryngeal lesions may have multiple etiologies with similar appearance and presentation.

More recent investigation into defense mechanisms against refluxed acid in the larynx and surrounding tissues suggests a possible mechanism of increased susceptibility in some patient populations. Defense mechanisms in the epithelium of the esophagus and larynx are known to differ. Active bicarbonate production is pumped into the extracellular space in the esophagus but not into the larynx. Recent investigations suggest that laryngeal tissues are protected from reflux damage by a carbonic anhydrase in the mucosa of the posterior larynx. The carbonic anhydrase enzyme catalyzes hydration of carbon dioxide to produce bicarbonate, which neutralizes the acid in refluxate. Carbonic anhydrase isoenzyme III, expressed at high levels in normal laryngeal epithelium, was shown to be absent in 64% of biopsy specimens from laryngeal tissues of laryngopharyngeal reflux (LPR) patients.8

Despite the common understating that reflux of acid causes respiratory symptoms, a recent prospective study from Sweden found that a 10-year follow-up of individuals with esophageal and pharyngeal acid exposure did  not correlate with increase risk of airway symptoms or laryngeal abnormalities.9

Frequency

United States

GERD is one of the most common disorders; US population surveys, for example, suggest that as many as 50% of adults (or 60 million people) have symptoms of heartburn at least once a month. More than one quarter of adult Americans use antacids 3 or more times per month. Although nearly half of the US population experiences occasional heartburn, only 4-7% report daily symptoms. This group of patients most likely represents those with significant esophageal complications of reflux disease.

The true incidence of GERD might be underestimated because of the relatively low proportion of individuals who seek medical attention for reflux symptoms. One report found that only 5% of patients with symptoms of heartburn and regurgitation had visited a physician because of this problem within the preceding year. An estimated 4-10% of chronic nonspecific laryngeal disorders in otolaryngology clinics are associated with reflux disease.

A recent retrospective review showed a significant increase in US ambulatory care visits for GERD, from a rate of 1.7 per 100 to 4.7 per 100 over 12 years. Otolaryngologists appeared to have an increasingly prominent role in management of this disease.10

Mortality/Morbidity

Symptoms of laryngopharyngeal reflux are more prevalent in patients with esophageal adenocarcinoma (EAC) than typical GERD symptoms and may represent the only sign of disease. Chronic cough is an independent risk factor associated with the presence of EAC.5 Therefore, laryngopharyngeal reflux (LPR) symptoms should be assessed in the screening for esophageal cancers and Barrett esophagus. Laryngopharyngeal reflux (LPR) may be a significant risk factor for the development of EAC.

Chronic laryngopharyngeal reflux (LPR) is a risk factor for symptomatic subglottic stenosis, laryngeal malacia, laryngeal stenosis, and laryngeal carcinoma.

Race

No particular racial predilection reported.

Sex

A slightly higher prevalence in males than females may exist (55% vs 45%).

Age

The percentage of patients with GERD who are older than 44 years appears to be slowly growing.

Clinical

History

The most common symptoms used by ENT physicians to diagnose GERD-related laryngitis or laryngopharyngeal reflux (LPR) included globus, throat clearing, cough, and hoarseness; sore throat and dysphagia were considered less useful.11

The typical symptoms of laryngopharyngeal reflux (LPR), as listed above, can be caused by chronic irritation of the vocal cords due to overuse, smoking, alcohol, infection, and allergies and other environmental irritants.

Furthermore, history alone is often insufficient to elicit clues that suggest acid reflux as a cause of these symptoms. Most patients with suspected laryngeal complications of GERD may have no esophageal symptoms.

Most ENT physicians reported that they relied significantly more on symptoms, rather than on laryngoscopic signs, in diagnosing laryngopharyngeal reflux (LPR).

Belfasky et al (2002) published the self-administered 9-item reflux symptom index (RSI) to assist clinicians in documenting the presence and degree of laryngopharyngeal reflux (LPR) symptoms, both before and after treatment (see Image 1).12

The RSI documents the presence and degree of nine...

The RSI documents the presence and degree of nine laryngopharyngeal reflux (LPR) symptoms both before and after treatment; maximum score: 45.

[ CLOSE WINDOW ]
The RSI documents the presence and degree of nine...

The RSI documents the presence and degree of nine laryngopharyngeal reflux (LPR) symptoms both before and after treatment; maximum score: 45.


  • Supraesophageal
    • Globus (This was the primary symptom in 4% of visits and was unrelated to the severity of reflux symptoms in a large cohort of more than 4000 general otolaryngology clinic patients. Globus was not associated with any specific psychometric parameters in 88 gastroenterology clinic patients.)
    • A history of persistent throat clearing
    • Chronic cough
    • Halitosis
    • Recurrent or persistent hoarseness, especially in the morning
  • Esophageal symptoms associated with laryngopharyngeal reflux (LPR)  
    • Regurgitation: A history of regurgitation, particularly at nighttime, associated with cough or with symptoms suggesting aspiration is the most significant clue to the possibility of supraesophageal complications of GERD. Unfortunately, this symptom complex occurs in a minority of patients.
    • Heartburn: The presence of heartburn symptoms can be a significant indication, but it should be defined appropriately in terms of the specific location and description of these symptoms. In a study of a large number of patients with suspected otolaryngologic complications of GERD, only 43% had classic symptoms of heartburn, regurgitation, or dysphagia. Heartburn was reported by 72% of 50 patients with idiopathic hoarseness and normal laryngoscopic findings who were refractory to speech therapy. Overall, GERD was demonstrable in 40% of patients by either esophagraphy or a 24-hour ambulatory pH study.
    • Other classic GERD-related history findings: These include patient symptoms related to the intake of tomato-based and/or spicy foods. These types of questions are important screening tools. Patients should also be asked about the frequency of using over-the-counter antacids. Often, patients deny having heartburn but then respond positively to questioning regarding problems with specific food types and/or frequent use of antacids.

Physical

Visualization of the larynx and vocal cords for signs of laryngopharyngeal reflux (LPR) requires a laryngoscopic examination. The most useful signs of GERD-related laryngitis or laryngopharyngeal reflux (LPR) were reported to be erythema, edema, presence of posterior commissure bar, and cobblestoning, while pseudosulcus vocalis; ulcers; and ventricular obliteration, nodules, polyps, and leukoplakia were reported to be less useful.11

Pseudosulcus vocalis (see below) was shown to be reported in as many as 90% of laryngopharyngeal reflux (LPR) cases. In a separate study, pseudosulcus was show to have a 70% sensitivity and 77% specificity in patients with laryngopharyngeal reflux (LPR). This further supports that the presence of pseudosulcus vocalis is suggestive of laryngopharyngeal reflux (LPR).12

Helicobacter pylori bacteria could enter and colonize the nasopharyngeal cavity by gastroesophageal reflux and may elicit otitis, sinusitis, pharyngitis, or laryngitis.


Belfasky et al (2002) developed an 8-item clinical severity scale to document laryngopharyngeal reflux (LPR) findings during fiberoptic laryngoscopy, which are quantified as the reflux finding score (RFS; see Image 2). The following 8 items are assessed to aid in the diagnosis of laryngopharyngeal reflux (LPR):

  1. Pseudosulcus vocalis
  2. Ventricular obliteration
  3. Erythema/hyperemia
  4. Vocal fold edema
  5. Diffuse laryngeal edema
  6. Posterior commissure hypertrophy
  7. Granuloma/granulation
  8. Thick endolaryngeal mucus
  • Posterior laryngitis: The classic laryngeal physical findings of laryngopharyngeal reflux (LPR) reported in the otolaryngology literature are edema and erythema of the posterior commissure.
  • Pseudosulcus vocalis: The medial edge of the vocal cord appears to have a linear indentation due to diffuse infraglottic edema.
  • Vocal cord granuloma
  • Subglottic stenosis - Subglottic stenosis is a significant complication associated with chronic pharyngeal acid exposure.
  • Contact ulcer of larynx
  • Additional signs related to laryngopharyngeal reflux
    • Recurrent or refractory sinusitis: A recent study on the long-term outcome of adult patients who underwent functional endoscopic sinus surgery indicated that GERD predicted poor symptom relief.
    • Dental erosions: Patients have a smooth, glazed, dished-out appearance of the dentin on the lingual surfaces of the teeth. The deleterious effect of regurgitated gastric acid on the teeth has been suggested in reports dating back to the early 1970s. These include association of dental erosions with hiatal hernia, chronic vomiting, rumination, alcoholic gastritis, and regurgitation, as well as anorexia nervosa and bulimia. Dental erosions are defined as the loss of tooth substance by a chemical process that does not involve bacteria. Dental erosions are hard dished-out areas with a smooth and glistening base as opposed to the soft, dark, and jagged-edge lesions of dental caries. The prevalence of dental erosions in patients with GERD was reportedly 20-55%, in contrast to 2-18% in the general population.
    • Sandifer syndrome: The unique neck posture in Sandifer syndrome is a clue to acid reflux disease in infants or young children. This posture is an anatomic defense mechanism against repetitive acid reflux.

Causes

  • Retrograde reflux of gastric acid or other contents (ie, pepsin) or both into the supraesophageal aerodigestive tract with mucosal injury from direct contact
  • Damage to cilia from refluxate that leads to mucous stasis and chronic throat clearing and cough, with consequent symptoms of laryngeal inflammation and irritation
  • Gastroesophageal reflux that leads to neurally mediated chronic cough and throat clearing with consequent symptoms with or without tissue injury
  • A defect in carbonic anhydrase isoenzyme III
  • Deglutitive pharyngolaryngeal abnormalities that lead to abnormal laryngeal exposure to contents transported in antegrade direction (possible role of defective airway protective defense mechanisms)

More on Reflux Laryngitis

Overview: Reflux Laryngitis
Differential Diagnoses & Workup: Reflux Laryngitis
Treatment & Medication: Reflux Laryngitis
Follow-up: Reflux Laryngitis
Multimedia: Reflux Laryngitis
References
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References

  1. Cherry J, Margulies SI. Contact ulcer of the larynx. Laryngoscope. Nov 1968;78(11):1937-40. [Medline].

  2. Koufman JA. The otolaryngologic manifestations of gastroesophageal reflux disease (GERD): a clinical investigation of 225 patients using ambulatory 24-hour pH monitoring and an experimental investigation of the role of acid and pepsin in the development of laryngeal injury. Laryngoscope. Apr 1991;101(4 Pt 2 Suppl 53):1-78. [Medline].

  3. Ford CN. Evaluation and management of laryngopharyngeal reflux. JAMA. Sep 28 2005;294(12):1534-40. [Medline].

  4. Maronian NC, Azadeh H, Waugh P, Hillel A. Association of laryngopharyngeal reflux disease and subglottic stenosis. Ann Otol Rhinol Laryngol. Jul 2001;110(7 Pt 1):606-12. [Medline].

  5. Reavis KM, Morris CD, Gopal DV, Hunter JG, Jobe BA. Laryngopharyngeal reflux symptoms better predict the presence of esophageal adenocarcinoma than typical gastroesophageal reflux symptoms. Ann Surg. Jun 2004;239(6):849-56; discussion 856-8. [Medline].

  6. Burton LK Jr, Murray JA, Thompson DM. Ear, nose, and throat manifestations of gastroesophageal reflux disease. Complaints can be telltale signs. Postgrad Med. Feb 2005;117(2):39-45. [Medline].

  7. Milstein CF, Charbel S, Hicks DM, Abelson TI, Richter JE, Vaezi MF. Prevalence of laryngeal irritation signs associated with reflux in asymptomatic volunteers: impact of endoscopic technique (rigid vs. flexible laryngoscope). Laryngoscope. Dec 2005;115(12):2256-61. [Medline].

  8. Gill GA, Johnston N, Buda A, Pignatelli M, Pearson J, Dettmar PW. Laryngeal epithelial defenses against laryngopharyngeal reflux: investigations of E-cadherin, carbonic anhydrase isoenzyme III, and pepsin. Ann Otol Rhinol Laryngol. Dec 2005;114(12):913-21. [Medline].

  9. Andersson O, Moller RY, Finizia C, Ruth M. A more than 10-year prospective, follow-up study of esophageal and pharyngeal acid exposure, symptoms and laryngeal findings in healthy, asymptomatic volunteers. Scand J Gastroenterol. 2009;44(1):23-31. [Medline].

  10. Altman KW, Stephens RM, Lyttle CS, Weiss KB. Changing impact of gastroesophageal reflux in medical and otolaryngology practice. Laryngoscope. Jul 2005;115(7):1145-53. [Medline].

  11. Ahmed TF, Khandwala F, Abelson TI, et al. Chronic laryngitis associated with gastroesophageal reflux: prospective assessment of differences in practice patterns between gastroenterologists and ENT physicians. Am J Gastroenterol. Mar 2006;101(3):470-8. [Medline].

  12. Belafsky PC, Postma GN, Koufman JA. The association between laryngeal pseudosulcus and laryngopharyngeal reflux. Otolaryngol Head Neck Surg. Jun 2002;126(6):649-52. [Medline].

  13. Malhotra A, Freston JW, Aziz K. Use of pH-impedance testing to evaluate patients with suspected extraesophageal manifestations of gastroesophageal reflux disease. J Clin Gastroenterol. Mar 2008;42(3):271-8. [Medline].

  14. So JB, Zeitels SM, Rattner DW. Outcomes of atypical symptoms attributed to gastroesophageal reflux treated by laparoscopic fundoplication. Surgery. Jul 1998;124(1):28-32. [Medline].

  15. Cadiere GB, Houben JJ, Bruyns J, Himpens J, Panzer JM, Gelin M. Laparoscopic Nissen fundoplication: technique and preliminary results. Br J Surg. Mar 1994;81(3):400-3. [Medline].

  16. Chambers DW, Davis WE, Cook PR, Nishioka GJ, Rudman DT. Long-term outcome analysis of functional endoscopic sinus surgery: correlation of symptoms with endoscopic examination findings and potential prognostic variables. Laryngoscope. Apr 1997;107(4):504-10. [Medline].

  17. Curran AJ, Barry MK, Callanan V, Gormley PK. A prospective study of acid reflux and globus pharyngeus using a modified symptom index. Clin Otolaryngol Allied Sci. Dec 1995;20(6):552-4. [Medline].

  18. Deveney CW, Benner K, Cohen J. Gastroesophageal reflux and laryngeal disease. Arch Surg. Sep 1993;128(9):1021-5; discussion 1026-7. [Medline].

  19. Dobhan R, Castell DO. Normal and abnormal proximal esophageal acid exposure: results of ambulatory dual-probe pH monitoring. Am J Gastroenterol. Jan 1993;88(1):25-9. [Medline].

  20. el-Serag HB, Sonnenberg A. Comorbid occurrence of laryngeal or pulmonary disease with esophagitis in United States military veterans. Gastroenterology. Sep 1997;113(3):755-60. [Medline].

  21. Farkkila MA, Ertama L, Katila H, Kuusi K, Paavolainen M, Varis K. Globus pharyngis, commonly associated with esophageal motility disorders. Am J Gastroenterol. Apr 1994;89(4):503-8. [Medline].

  22. First multi-disciplinary international symposium on supraesophageal complications of gastroesophageal reflux disease. Workshop consensus reports. Am J Med. Nov 24 1997;103(5A):149S-150S. [Medline].

  23. Gallup Organizational National Survey. Heartburn Across America. Princeton, NJ: The Gallup Organization Inc; 1988.

  24. Graham DY, Smith JL, Patterson DJ. Why do apparently healthy people use antacid tablets?. Am J Gastroenterol. May 1983;78(5):257-60. [Medline].

  25. Grossman TW, Toohill RJ, Mushtag E, et al. Pharyngeal, laryngeal and tracheobronchial manifestations of gastroesophageal reflux. Proceedings of the XXIV World Congress of Otolaryngology Head and Neck Surgery. Berkley, Calif: Kugler and Ghedini Publishing.

  26. Hanson DG. Diagnosis and management of chronic irritative laryngitis. Am J Med. 1999.

  27. Hanson DG, Jiang JJ, Chen J, Pauloski BR. Acoustic measurement of change in voice quality with treatment for chronic posterior laryngitis. Ann Otol Rhinol Laryngol. Apr 1997;106(4):279-85. [Medline].

  28. Hanson DG, Kamel PL, Kahrilas PJ. Outcomes of antireflux therapy for the treatment of chronic laryngitis. Ann Otol Rhinol Laryngol. Jul 1995;104(7):550-5. [Medline].

  29. Helm JF, Shaker R, Dodds WJ. Revelations about ambulatory esophageal pH monitoring. Gastroenterology. 1988;94(5):A421.

  30. Hill J, Stuart RC, Fung HK, et al. Gastroesophageal reflux, motility disorders, and psychological profiles in the etiology of globus pharyngis. Laryngoscope. Oct 1997;107(10):1373-7. [Medline].

  31. Howden GF. Erosion as the presenting symptom in hiatus hernia. A case report. Br Dent J. Nov 16 1971;131(10):455-6. [Medline].

  32. Jacob P, Kahrilas PJ, Herzon G. Proximal esophageal pH-metry in patients with 'reflux laryngitis'. Gastroenterology. Feb 1991;100(2):305-10. [Medline].

  33. Jamieson GG, Watson DI, Britten-Jones R, Mitchell PC, Anvari M. Laparoscopic Nissen fundoplication. Ann Surg. Aug 1994;220(2):137-45. [Medline].

  34. Jarvinen V, Meurman JH, Hyvarinen H, Rytomaa I, Murtomaa H. Dental erosion and upper gastrointestinal disorders. Oral Surg Oral Med Oral Pathol. Mar 1988;65(3):298-303. [Medline].

  35. Jindal JR, Milbrath MM, Shaker R, Hogan WJ, Toohill RJ. Gastroesophageal reflux disease as a likely cause of "idiopathic" subglottic stenosis. Ann Otol Rhinol Laryngol. Mar 1994;103(3):186-91. [Medline].

  36. Jones NS, Lannigan FJ, McCullagh M, et al. Acid reflux and hoarseness. J Voice. 1990;4(4):355-58.

  37. Kambic V, Radsel Z. Acid posterior laryngitis. Aetiology, histology, diagnosis and treatment. J Laryngol Otol. Dec 1984;98(12):1237-40. [Medline].

  38. Kamel PL, Hanson D, Kahrilas PJ. Omeprazole for the treatment of posterior laryngitis. Am J Med. Apr 1994;96(4):321-6. [Medline].

  39. Katz PO. Ambulatory esophageal and hypopharyngeal pH monitoring in patients with hoarseness. Am J Gastroenterol. Jan 1990;85(1):38-40. [Medline].

  40. Katzka DA, Paoletti V, Leite L, Castell DO. Prolonged ambulatory pH monitoring in patients with persistent gastroesophageal reflux disease symptoms: testing while on therapy identifies the need for more aggressive anti-reflux therapy. Am J Gastroenterol. Oct 1996;91(10):2110-3. [Medline].

  41. Lazarchik DA, Filler SJ. Effects of gastroesophageal reflux on the oral cavity. Am J Med. Nov 24 1997;103(5A):107S-113S. [Medline].

  42. Locke GR 3rd, Talley NJ, Fett SL, Zinsmeister AR, Melton LJ 3rd. Prevalence and clinical spectrum of gastroesophageal reflux: a population-based study in Olmsted County, Minnesota. Gastroenterology. May 1997;112(5):1448-56. [Medline].

  43. Luostarinen M, Isolauri J, Laitinen J, et al. Fate of Nissen fundoplication after 20 years. A clinical, endoscopical, and functional analysis. Gut. Aug 1993;34(8):1015-20. [Medline].

  44. Lussi A, Schaffner M, Hotz P, Suter P. Dental erosion in a population of Swiss adults. Community Dent Oral Epidemiol. Oct 1991;19(5):286-90. [Medline].

  45. Mair IW, Natvig K, Maurer HJ, Odegaard HI. The globus symptom. ORL J Otorhinolaryngol Relat Spec. 1973;35(2):104-10. [Medline].

  46. McNally PR, Maydonovitch CL, Prosek RA, Collette RP, Wong RK. Evaluation of gastroesophageal reflux as a cause of idiopathic hoarseness. Dig Dis Sci. Dec 1989;34(12):1900-4. [Medline].

  47. Metz DC, Childs ML, Ruiz C, Weinstein GS. Pilot study of the oral omeprazole test for reflux laryngitis. Otolaryngol Head Neck Surg. Jan 1997;116(1):41-6. [Medline].

  48. Meurman JH, Toskala J, Nuutinen P, Klemetti E. Oral and dental manifestations in gastroesophageal reflux disease. Oral Surg Oral Med Oral Pathol. Nov 1994;78(5):583-9. [Medline].

  49. Miko TL. Peptic (contact ulcer) granuloma of the larynx. J Clin Pathol. Aug 1989;42(8):800-4. [Medline].

  50. Moloy PJ, Charter R. The globus symptom. Incidence, therapeutic response, and age and sex relationships. Arch Otolaryngol. Nov 1982;108(11):740-4. [Medline].

  51. Moser G, Vacariu-Granser GV, Schneider C, et al. High incidence of esophageal motor disorders in consecutive patients with globus sensation. Gastroenterology. Dec 1991;101(6):1512-21. [Medline].

  52. Ott DJ, Ledbetter MS, Koufman JA, Chen MY. Globus pharyngeus: radiographic evaluation and 24-hour pH monitoring of the pharynx and esophagus in 22 patients. Radiology. Apr 1994;191(1):95-7. [Medline].

  53. Peters JH, Heimbucher J, Kauer WK, Incarbone R, Bremner CG, DeMeester TR. Clinical and physiologic comparison of laparoscopic and open Nissen fundoplication. J Am Coll Surg. Apr 1995;180(4):385-93. [Medline].

  54. Pindborg JJ. Chemical and physical injuries. In: Pindborg JJ, ed. Pathology of the Dental Hard Tissues. Philadelphia, Pa: WB Saunders Co; 1970:312-25.

  55. Richter JE. Ambulatory esophageal pH monitoring. Am J Med. Nov 24 1997;103(5A):130S-134S. [Medline].

  56. Ruth M, Carlsson S, Mansson I, Bengtsson U, Sandberg N. Scintigraphic detection of gastro-pulmonary aspiration in patients with respiratory disorders. Clin Physiol. Jan 1993;13(1):19-33. [Medline].

  57. Schroeder PL, Filler SJ, Ramirez B, Lazarchik DA, Vaezi MF, Richter JE. Dental erosion and acid reflux disease. Ann Intern Med. Jun 1 1995;122(11):809-15. [Medline].

  58. Shaker R, Milbrath M, Ren J, et al. Esophagopharyngeal distribution of refluxed gastric acid in patients with reflux laryngitis. Gastroenterology. Nov 1995;109(5):1575-82. [Medline].

  59. Shaw GY, Searl JP, Young JL, Miner PB. Subjective, laryngoscopic, and acoustic measurements of laryngeal reflux before and after treatment with omeprazole. J Voice. Dec 1996;10(4):410-8. [Medline].

  60. Sognnaes RF, Wolcott RB, Xhonga FA. Dental erosion. I. Erosion-like patterns occurring in association with other dental conditions. J Am Dent Assoc. Mar 1972;84(3):571-6. [Medline].

  61. Thompson WG, Heaton KW. Heartburn and globus in apparently healthy people. Can Med Assoc J. Jan 1 1982;126(1):46-8. [Medline].

  62. Ulualp SO, Toohill RJ, Hoffmann R, Shaker R. Pharyngeal pH monitoring in patients with posterior laryngitis. Otolaryngol Head Neck Surg. May 1999;120(5):672-7. [Medline].

  63. Ulualp SO, Toohill RJ, Hoffmann R, Shaker R. Possible relationship of gastroesophagopharyngeal acid reflux with pathogenesis of chronic sinusitis. Am J Rhinol. May-Jun 1999;13(3):197-202. [Medline].

  64. Ulualp SO, Toohill RJ, Kern M, Shaker R. Pharyngo-UES contractile reflex in patients with posterior laryngitis. Laryngoscope. Sep 1998;108(9):1354-7. [Medline].

  65. Ulualp SO, Toohill RJ, Shaker R. Pharyngeal acid reflux in patients with single and multiple otolaryngologic disorders. Otolaryngol Head Neck Surg. Dec 1999;121(6):725-30. [Medline].

  66. Vaezi MF, Schroeder PL, Richter JE. Reproducibility of proximal probe pH parameters in 24-hour ambulatory esophageal pH monitoring. Am J Gastroenterol. May 1997;92(5):825-9. [Medline].

  67. Weusten BL, Akkermans LM, vanBerge-Henegouwen GP, Smout AJ. Spatiotemporal characteristics of physiological gastroesophageal reflux. Am J Physiol. Mar 1994;266(3 Pt 1):G357-62. [Medline].

  68. Wiener GJ, Koufman JA, Wu WC, Cooper JB, Richter JE, Castell DO. Chronic hoarseness secondary to gastroesophageal reflux disease: documentation with 24-h ambulatory pH monitoring. Am J Gastroenterol. Dec 1989;84(12):1503-8. [Medline].

  69. Wilson JA, Heading RC, Maran AG, Pryde A, Piris J, Allan PL. Globus sensation is not due to gastro-oesophageal reflux. Clin Otolaryngol Allied Sci. Aug 1987;12(4):271-5. [Medline].

  70. Wo JM, Grist WJ, Gussack G, Delgaudio JM, Waring JP. Empiric trial of high-dose omeprazole in patients with posterior laryngitis: a prospective study. Am J Gastroenterol. Dec 1997;92(12):2160-5. [Medline].

  71. Woo P, Noordzij P, Ross JA. Association of esophageal reflux and globus symptom: comparison of laryngoscopy and 24-hour pH manometry. Otolaryngol Head Neck Surg. Dec 1996;115(6):502-7. [Medline].

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Further Reading

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Keywords

refluxed gastric acid, supraesophageal gastroesophageal reflux disease, supraesophageal GERD, atypical gastroesophageal reflux disease, atypical GERD, laryngopharyngeal reflux, LPR, extraesophageal complications of gastroesophageal reflux disease, extraesophageal complications of GERD, chronic laryngeal disorder, pharyngolaryngeal manifestations of gastroesophageal reflux disease, pharyngolaryngeal manifestations of GERD, reflux-induced supraesophageal lesions, aerodigestive tract disorders, empiric antireflux treatment, abnormal esophageal acid exposure, recurrent hoarseness, persistent hoarseness, persistent throat clearing, halitosis, hypersialorrhea, globus, regurgitation, heartburn, dysphagia, posterior laryngitis, contact ulcer of larynx, pachyderma laryngis, vocal cord granuloma, subglottic stenosis, recurrent mouth ulcers, idiopathic pulmonary fibrosis, recurrent noninfectious pulmonary infiltrates, recurrent sinusitis, refractory sinusitis, dental erosions, Sandifer syndrome

deglutitive dysfunction, neurally mediated chronic cough, reflux laryngitis

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Contributor Information and Disclosures

Author

Bardia Amirlak, MD, Fellow, Department of Plastic and Reconstructive Surgery, Case Western School of Medicine
Bardia Amirlak, MD is a member of the following medical societies: American Medical Association and American Society of Reconstructive Transplantation
Disclosure: Nothing to disclose.

Coauthor(s)

Pamela A Mudd, BS, MD, Resident Physician, Department of Otolaryngology, University of Colorado Health Science Center
Pamela A Mudd, BS, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery and American College of Physicians
Disclosure: Nothing to disclose.

Reza Shaker, MD, Chief, Professor, Department of Internal Medicine, Division of Gastroenterology and Hepatology, Medical College of Wisconsin
Reza Shaker, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Federation for Medical Research, American Gastroenterological Association, American Motility Society, American Physiological Society, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

Medical Editor

Clark A Rosen, MD, Director, University of Pittsburgh Voice Center; Associate Professor, Department of Otolaryngology and Communication Science and Disorders, University of Pittsburgh School of Medicine
Clark A Rosen, MD is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Medical Association, and Pennsylvania Medical Society
Disclosure: Bioform Medical  Consulting fee Consulting

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Robert M Kellman, MD, Professor and Chair, Department of Otolaryngology and Communication Sciences, State University of New York, Upstate Medical University
Robert M Kellman, MD is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Medical Association, American Neurotology Society, American Rhinologic Society, American Society for Head and Neck Surgery, Medical Society of the State of New York, and Triological Society
Disclosure: GE Healthcare Honoraria Review panel membership

CME Editor

Christopher L Slack, MD, Otolaryngology-Facial Plastic Surgery, Private Practice, Associated Coastal ENT; Medical Director, Treasure Coast Sleep Disorders
Christopher L Slack, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Arlen D Meyers, MD, MBA, Professor, Department of Otolaryngology-Head and Neck Surgery, University of Colorado School of Medicine
Arlen D Meyers, MD, MBA is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, and American Head and Neck Society
Disclosure: Covidien Corp Consulting fee Consulting; US Tobacco Corporation unstricted gift unknown

 
 
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