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Symptoms and findings of laryngopharyngeal reflux.

Abstract

Even though the symptoms and findings of laryngopharyngeal reflux (LPR) have been described, the clinical diagnosis is sometimes elusive. Symptoms can occur in the absence of conclusive laryngeal physical findings, and they can be nonspecific. For example, dysphonia can be caused not only by LPR, but also by neoplasia and by geriatric, neurologic, and behavioral disorders. The clinician must realize that the diagnosis of LPR is based on a combination of factors, including symptoms, laryngeal findings, and diagnostic test results.

Symptoms

There are more than a dozen common symptoms of LPR (table). We have developed and previously published the self-administered nine-item reflux symptom index (RSI) to assist clinicians in documenting the presence and degree of LPR symptoms, both before and after treatment (figure 1). (1,2) This instrument appears to be valid and highly reproducible. (1)

In addition to typical LPR symptoms, reflux-induced respiratory symptoms are also common. The association between LPR and asthma has been well documented. (3-5) Nearly 70% of asthmatics exhibit reflux symptoms and abnormal results on pH monitoring; LPR is silent in as many as one-quarter of patients with difficult-to-control asthma. (3-5)

Microaspiration of gastric refluxate and resultant bronchiectasis can also occur. Some investigators have found strong associations between LPR and airway stenosis, sleep apnea, laryngospasm, and nasal congestion. (6-15) Although the etiology of these disorders is multifactorial, LPR as a sole cause or as a cofactor should be routinely considered in the differential diagnosis of subglottic stenosis, asthma, laryngospasm, bronchiectasis, chronic rhinitis, and sleep-disordered breathing.

Findings

The classic laryngeal physical findings of LPR reported in the otolaryngology literature are edema and erythema of the posterior commissure--so-called posterior laryngitis. (16-19) In reality, however, LPR can cause an array of findings that range from mild edema of the true vocal folds to diffuse airway inflammation and stenosis.

We have developed an eight-item clinical severity scale to document LPR findings during fiberoptic laryngoscopy, which are quantified as the reflux finding score (RFS) (figure 2). (20) The eight items were derived from a pool of the most common laryngeal findings in LPR patients seen at our voice center. They are (1) pseudosulcus vocalis, (2) ventricular obliteration, (3) erythema/hyperemia, (4) vocal fold edema, (5) diffuse laryngeal edema, (6) posterior commissure hypertrophy, (7) granuloma/ granulation, and (8) thick endolaryngeal mucus.

Pseudosulcus vocalis. One of the most common laryngeal findings of LPR is pseudosulcus vocalis (figure 3). This term is rather self-descriptive, and it refers to edema of the undersurface of the vocal fold that extends from the anterior commissure to the posterior larynx and creates the appearance of a groove or sulcus. A vocal fold with pseudosulcus has been described as having the appearance of a partially open hot-dog bun. This finding is also referred to as subglottic edema, even though the edema is not really subglottic.

Pseudosulcus can be easily differentiated from true sulcus vergeture (adherence of the vocal fold epithelium to the underlying vocal ligament) that has been caused by scarring. While true sulcus stops at the vocal process and is found in the striking zone, pseudosulcus vocalis extends all the way to the back of the larynx and is located inferior to the striking zone. Recent clinical reports suggest that the positive predictive value of pseudosulcus for LPR might be as high as 90%, and that its sensitivity and specificity are 70% and 77%, respectively. (21,22)

In the aging larynx, pseudosulcus can be seen without LPR. In this instance, the appearance of pseudosulcus is the result of droopy, relatively inelastic vocal fold epithelium draped over thin, atrophic vocal fold musculature. Fortunately, pseudosulcus as the only finding is rare in LPR. In other words, LPR patients usually have several LPR findings. Thus, with the exception of isolated pseudosulcus in the elderly, the presence of pseudosulcus is highly suggestive of LPR.

Ventricular obliteration. The laryngeal ventricle is the space between the true and false vocal folds. When both sets of vocal folds become swollen, this space can become diminished or completely obliterated (figure 4). With ventricular obliteration, the medial edge of the ventricular bands usually becomes broad and swollen. (20)

With the RFS scale, ventricular obliteration is graded as partial or complete. Ventricular obliteration is an important LPR finding. With effective antireflux treatment, the obliteration diminishes noticeably, and the ventricular bands become sharp and angular.

Erythema/hyperemia. Although reports in the otolaryngology literature are split regarding the prevalence and significance of redness associated with LPR, it is our opinion that regardless of the severity of LPR, erythema and/or hyperemia are present in fewer that half of all cases. Redness is not usually diagnostic of LPR. (20)

Although an attempt has been made to quantify laryngeal erythema, the evaluation of redness on endoscopy is often difficult and depends on the type of endoscope, light source, and video monitor utilized. (23) Because of this limitation, we choose to classify laryngeal erythema as localized to the arytenoids only or diffuse when it affects the entire larynx.

Vocal fold edema. Clinically, we have noted that a small degree of true vocal fold edema can have a dramatic effect on the voice. In LPR, vocal fold edema can range from mild to end-stage polypoid degeneration (figure 5). Grade 1 edema is characterized by rounding of the free edges, and grade 2 by pseudosulcus. Grade 3 edema features sessile changes, and grade 4 represents polypoid degeneration (Reinke's edema).

Diffuse laryngeal edema. The presence of diffuse laryngeal edema is a somewhat subjective parameter and refers to the relative ratio of the endolaryngeal airway to the whole larynx. Grade 1 denotes any degree of diffuse laryngeal edema. In grade 2 laryngeal edema, the lumen is encroached, usually by posterior laryngeal hypertrophy. Grade 3 represents diffuse pachydermia laryngis ("elephant skin" of the larynx), wherein the ratio of the airway to the overall laryngeal diameter is less than one-half. Grade 4 denotes some degree of clinical airway obstruction.

Posterior commissure hypertrophy. Mucosal hypertrophy of the posterior commissure epithelium is graded as mild when there is a mustache-like appearance of the posterior commissure mucosa, moderate when the posterior commissure is swollen enough to create a straight line across the back of the larynx, severe when there is bulging of the posterior larynx into the airway, and obstructing when a significant portion of the airway is obliterated (figure 6).

Granuloma/granulation. Granuloma or granulation tissue anywhere in the larynx is graded as a positive LPR finding (figure 7).

Thick endolaryngeal mucus. Thick, white endolaryngeal mucus on the vocal folds or elsewhere in the endolarynx is graded as a positive physical finding.
Figure 1

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

The reflux symptom index

Within the past month, how did the 0 = No Problem
following problems affected you? 5 = Severe Problem

Hoarseness or a problem with your voice 0 1
Clearing your throat 0 1
Excess throat mucus or postnasal drip 0 1
Difficulty swallowing food, liquids, or pills 0 1
Coughing after you ate or after lying down 0 1
Breathing difficulties or choking episodes 0 1
Troublesome or annoying cough 0 1
Sensations of something sticking in your throat
or a lump in your throat 0 1
Heartburn, chest pain, indigestion, or stomach 0 1
acid coming up

Total

Within the past month, how did the 0 = No Problem
following problems affected you? 5 = Severe Problem

Hoarseness or a problem with your voice 2 3
Clearing your throat 2 3
Excess throat mucus or postnasal drip 2 3
Difficulty swallowing food, liquids, or pills 2 3
Coughing after you ate or after lying down 2 3
Breathing difficulties or choking episodes 2 3
Troublesome or annoying cough 2 3
Sensations of something sticking in your throat
or a lump in your throat 2 3
Heartburn, chest pain, indigestion, or stomach 2 3
acid coming up

Total

Within the past month, how did the 0 = No Problem
following problems affected you? 5 = Severe Problem

Hoarseness or a problem with your voice 4 5
Clearing your throat 4 5
Excess throat mucus or postnasal drip 4 5
Difficulty swallowing food, liquids, or pills 4 5
Coughing after you ate or after lying down 4 5
Breathing difficulties or choking episodes 4 5
Troublesome or annoying cough 4 5
Sensations of something sticking in your throat
or a lump in your throat 4 5
Heartburn, chest pain, indigestion, or stomach 4 5
acid coming up

Total
Figure 2

The RFS documents the presence and degree of eight LPR findings during
fiberoptic laryngoscopy; maximum socre: 26.

The reflux finding score

Pseudosulcus (infraglottic edema) 0 = Absent
 2 = Present

Ventricular obliteration 0 = None
 2 = Partial
 4 = Complete

Erythema/hyperemia 0 = None
 2 = Arytenoids only
 4 = Diffuse

Vocal fold edema 0 = None
 1 = Mild
 2 = Moderate
 3 = Severe
 4 = Polypoid

Diffuse laryngeal edema 0 = None
 1 = Mild
 2 = Moderate
 3 = Severe
 4 = Obstructing

Posterior commissure hypertrophy 0 = None
 1 = Mild
 2 = Moderate
 3 = Severe
 4 = Obstructing

Granuloma/granulation 0 = Absent
 2 = Present

Thick endolaryngeal mucus 0 = Absent
 2 = Present

Total
Table

Common symptoms of LPR in approximate order of incidence

Chronic dysphonia
Intermittent dysphonia
Vocal fatigue
Voice breaks
Chronic throat clearing
Excessive throat mucus
Postnasal drip
Chronic cough
Dysphagia
Globus pharyngeus
Heartburn
Regurgitation
Airway obstruction
Paroxysmal laryngospasm
Wheezing


References

(1.) Belafsky PC, Postma GN, Koufman JA. Laryngopharyngeal reflux symptoms improve before changes in physical findings. Laryngoscope 2001;111:979-81.

(2.) Belafsky PC, Postma GN, Koufman JA. Validity and reliability of the reflux symptom index (RSI). J Voice 2002;16:274-7.

(3.) Field SK, Underwood M, Brant R, Cowie RL. Prevalence of gastroesophageal reflux symptoms in asthma. Chest 1996;109:316-22.

(4.) Harding SM, Guzzo MR. Richter JE. 24-h esophageal pH testing in asthmatics: Respiratory symptom correlation with esophageal acid events. Chest 1999:115:654-9.

(5.) Irwin RS, Curley FJ, French CL. Difficult-to-control asthma. Contributing factors and outcome of a systematic management protocol. Chest 1993;103:1662-9.

(6.) DiBaise JK, Olusola BF, Huerter JV, Quigley EM. Ro]e of GERD in chronic resistant sinusitis: A prospective, open label, pilot trial. Am J Gastroenterol 2002;97:843-50.

(7.) Loehrl TA, Smith TL, Darling RJ, et al. Autonomic dysfunction, vasomotor rhinitis, and extraesophageal manifestations of gastroesophageal reflux. Otolaryngol Head Neck Surg 2002;126:382-7.

(8.) 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 1991;101(Suppl 53):1-78.

(9.) Little FB, Koufman JA, Kohut RI, Marshall RB. Effect of gastric acid on the pathogenesis of subglottic stenosis. Ann Otol Rhinol Laryngol 1985;94:516-9.

(10.) Maronian NC, Azadeh H, Waugh P, Hillel A. Association of laryngopharyngeal reflux disease and subglottic stenosis. Ann Otol Rhinol Laryngol 2001;l10:606-12.

(11.) Loughlin CJ, Koufman JA. Paroxysmal laryngospasm secondary to gastroesophageal reflux. Laryngoscope 1996;106:1502-5.

(12.) Jindal JR. Milbrath MM, Shaker R, et al. Gastroesophageal reflux disease as a likely cause of "idiopathic" subglottic stenosis. Ann Otol Rhinol Laryngol 1994;103:186-91.

(13.) Valipour A, Makker HK, Hardy R, et al. Symptomatic gastroesophageal reflux in subjects with a breathing sleep disorder. Chest 2002;121:1748-53.

(14.) Senior BA. Khan M, Schwimmer C, et al. Gastroesophageal reflux and obstructive sleep apnea. Laryngoscope 2001;111:2144-6.

(15.) Konermann M, Radu HJ, Teschler H, et al. Interaction of sleep disturbances and gastroesophageal reflux in chronic laryngitis. Am J Otolaryngol 2002:23:20-6.

(16.) Cherry J, Margulies SI. Contact ulcer of the larynx. Laryngoscope 1968;78:1937-40.

(17.) Delahunty JE, Cherry J. Experimentally produced vocal cord granulomas. Laryngoscope 1968;78:1941-7.

(18.) Habermann W, Eherer A, Lindbichler F, et al. Ex juvantibus approach for chronic posterior laryngitis: Results of short-term pantoprazole therapy. J Laryngol Otol 1999;113:734-9.

(19.) Ulualp SO, Toohill RJ, Hoffmann R, Shaker R. Pharyngeal pH monitoring in patients with posterior laryngitis. Otolaryngol Head Neck Surg 1999:120:672-7.

(20.) Belafsky PC, Postma GN, Koufman JA. The validity and reliability of the reflux finding score (RFS). Laryngoscope 2001;111:1313-7.

(21.) Hickson C, Simpson CB, Falcon R. Laryngeal pseudosulcus as a predictor of laryngopharyngeal reflux. Laryngoscope 2001;111:1742-5.

(22.) Belafsky PC, Postma ON, Koufman JA. The association between laryngeal pseudosulcus and laryngopharyngeal reflux. Otolaryngol Head Neck Surg 2002;126:649-52.

(23.) Hanson DG, Jiang J, Chi W. Quantitative color analysis of laryngeal erythema in chronic posterior laryngitis. J Voice 1998;12:78-83.
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Article Details
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Author:Koufman, James A.
Publication:Ear, Nose and Throat Journal
Geographic Code:1USA
Date:Sep 1, 2002
Words:2077
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