Abnormal Endoscopic Pharyngeal and Laryngeal

Findings Attributable to Reflux

Peter C. Belafsky, MD, PhD

The symptom complex associated with acid-induced

injury to the larynx is referred to as laryngopharyngeal reflux (LPR). Basing the diagnosis of LPR on
patient symptoms or 24-hour dual-probe pH data
may be inaccurate, as these diagnostic tests are
restricted by limitations in both sensitivity and specificity. The clinician must have a thorough understanding of endoscopic findings associated with this
disorder. The severity of laryngeal inflammation
caused by acid and activated pepsin can be quantified. This article reviews the abnormal endoscopic
pharyngeal and laryngeal findings that are attributable to reflux. Am J Med. 2003;115(3A):90S96S.
2003 by Excerpta Medica, Inc.

he posterior aspect of the glottis makes up 5% of

the entire larynx. Although reflux-induced injury
to the larynx is often referred to as posterior laryngitis, this term is inaccurate because it disregards the
majority of laryngeal tissue injury that results from reflux.
Although several names have been suggested for refluxinduced laryngeal disorders (Table 1), laryngopharyngeal reflux (LPR) is the nomenclature adopted by the
American Academy of OtolaryngologyHead and Neck
Surgery, and will be used throughout this discussion.1
Symptoms attributed to LPR include hoarseness, cough,
dysphagia, globus, chronic throat clearing, and postnasal
drip. However, these symptoms are not specific for LPR,
and may be caused by rhinitis, asthma, laryngeal cancer,
and many other pathologic conditions. The nonspecific
nature of these symptoms has led many to regard dualprobe (distal and proximal) 24-hour pH monitoring as
the current gold standard for the diagnosis of LPR.
LPR is intermittent, however, and the sensitivity of extraesophageal reflux testing is estimated to be at best 80%.
This limitation, along with the observation that hypopharyngeal reflux occurs to a certain degree in normal individuals, has caused some researchers to question the clinical accuracy of this diagnostic test. The limitations of
patient symptoms and pH testing in diagnosing LPR has
motivated other investigators to quantify laryngeal findings attributed to reflux. These laryngeal findings are the
focus of this review.

EVALUATING LARYNGOPHARYNGEAL
REFLUX

From the Scripps Center for Voice and Swallowing, La Jolla, California,
USA.
Requests for reprints should be addressed to Peter C. Belafsky, MD,
PhD, Scripps Center for Voice and Swallowing, 9834 Genesee Avenue,
Suite 128, La Jolla, Calfornia 92037.
90S

2003 by Excerpta Medica, Inc.

All rights reserved.

Because no validated instrument existed previously to

perform a quantitative evaluation of LPR, we validated an
8-item reflux finding score (RFS) (Table 2) based on
physical findings observed during fiberoptic endoscopy.2
The RFS was developed to standardize the clinical findings of LPR so that clinicians may better diagnose, document symptom severity, and assess therapeutic efficacy of
patients with this disorder. The instrument ranges from a
minimum score of zero (no inflammation) to a maximum score of 26. It is important to note that the finding
score is simply a clinical scale of laryngeal inflammation.
The independent items on the RFS are not meant to individually predict the presence or absence of LPR. In addition, other sources of laryngeal inflammation such as
infection, allergy, neoplasia, autoimmune disorders, and
environmental toxins can result in an abnormal RFS.
0002-9343/03/$22.00
doi:10.1016/S0002-9343(03)00204-3

A Symposium: Abnormal Endoscopic Pharyngeal and Laryngeal Findings Attributable to Reflux/Belafsky

Table 1. Terms Used to Describe Reflux-Induced Laryngeal

Disorders
Laryngopharyngeal reflux
Posterior laryngitis
Gastroesopharyngeal reflux
Esophagopharyngeal reflux
Reflux laryngitis
Gastroesophageallaryngeal reflux
Supraesophageal reflux
Pharyngoesophageal reflux
Extraesophageal reflux

TRUE VOCAL FOLD FINDINGS

Table 2. Reflux Finding Score (RFS)

Condition

fold lesions are shown in Figure 1. Differential diagnoses

may apply to the location of the finding (localized vs. diffuse,
true vs. false vocal folds), characteristics of vocal fold edema
and erythema, type of lesion (cysts, nodules, polyps, granulomas), and associated clinical symptoms.

RFS

Subglottic edema

0 absent
2 present

Ventricular obliteration

0 none
2 partial
4 complete

Erythema/hyperemia

0 none
2 arytenoids only
4 diffuse

Vocal cord 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

In the same study,2 we assessed 40 patients with LPR

confirmed by double-probe pH monitoring at pretreatment and at 2, 4, and 6 months posttreatment. We also
examined 40 larynges in asymptomatic individuals. The
mean RFS for the normal individuals was 5.2 (95% confidence interval, 3.6 6.8), while the mean RFS for patients with confirmed LPR was 11.5 (5.2 SD). Thus,
subtle findings of LPR appear to be ubiquitous, and we
determined that an RFS 6 should be considered normal.2 Nonetheless, the RFS is reproducible, reliable, and
accurately documents treatment efficacy among patients
with LPR. It provides a useful framework for describing
reflux-induced laryngeal tissue injury.

ENDOSCOPIC LARYNGEAL FINDINGS

Determining the relation between endoscopic findings and
LPR can be a complex task. Clinical findings related to vocal

Edema of the true vocal fold ranges from mild swelling of

the mucosal surface to polypoid degeneration (Reinke
edema). Reinke edema is characterized by the accumulation of mucoid material in the Reinke space (superficial
layer of the lamina propria). The disease has been attributed to LPR, tobacco, and vocal misuse.3,4 Indeed, at least
1 study found that the primary cause for Reinke edema
and its recurrence was tobacco use.3 A localized area of
unilateral Reinke edema is sometimes referred to as a
pseudocyst. It frequently occurs on the middle of the free
edge of the vocal fold striking zone. Unlike traditional
Reinke edema, which is bilateral, a pseudocyst is unilateral and is associated with vocal fold paresis, not inflammation. It is believed to be the result of asymmetric shearing forces during mucosal vibration.5 Thus, the finding of
unilateral Reinke edema or pseudocyst should alert the
clinician to the likelihood of vocal cord paresis.
A laryngeal polyp, in comparison with a pseudocyst, is
a projecting or pedunculated mass of hypertrophied mucosa, usually with a stalk. A vocal fold cyst tends to have a
true capsule, and occurs in a slightly deeper plane of the
lamina propria than a polyp. These lesions are typically
unilateral and can be confused with vocal fold nodules
that are symmetric and bilateral. In comparison with the
slightly deeper cysts and polyps, vocal nodules do not
alter vocal fold mucosal vibration.
Although some investigators have reported a strong relation between laryngeal erythema and LPR,6 laryngeal erythema is a relatively nonspecific finding that is significantly
dependent on the examiners videoendoscopic equipment.
Subtle changes in color characteristics (color value, hue, saturation, and brightness) associated with erythema are difficult to quantify, and vary depending on the quality of the
fiberscope, video monitor, printer, and light source. Nonetheless, laryngeal erythema can be classified as isolated when
confined to the mucosa overlying the arytenoid and corniculate cartilages and diffuse when involving the entire larynx.
Compared with localized erythema, diffuse erythema is
more likely to be associated with reflux. Localized erythema
contributes 2 points to the RFS, and diffuse laryngeal erythema contributes 4 points.

NONVOCAL FOLD LARYNGEAL

FINDINGS
The space between the true and false vocal folds is known
as the laryngeal ventricle. Swelling of the true and false
vocal folds causes this space to be poorly visualized (oblit-

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Figure 1. Clinical findings related to vocal fold lesions. (A) Normal larynx and subglottis. (B) Localized area of Reinke edema
(pseudocyst) on striking zone of right vocal fold. (C) Bilateral Reinke edema. Also present are posterior commissure hypertrophy,
complete ventricular obliteration, diffuse laryngeal edema, and hyperemia. (D) Vocal fold polyp obscuring anterior two thirds of
glottis. (E) Vocal fold nodules (bilateral) at junction of anterior and middle one third of the vocal fold. (F) Right encapsulated,
subepithelial vocal fold cyst.

Figure 2. Appearance of the laryngeal ventricle, or space between the true and false vocal folds. (A) Open laryngeal ventricles
(arrows). (B) Obliterated laryngeal ventricles. Also present are mild posterior commissure hypertrophy mustacheing and moderate
vocal fold edema.
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erated). This finding may be noted in up to 80% of persons with pH-documented LPR, and is noticeably reversed with successful antireflux treatment.2 With partial
ventricular obliteration, the ventricular space is reduced
and the false vocal fold edge is indistinct. With complete
ventricular obliteration, the true and false vocal folds appear to touch, and there is no true ventricular space (Figure 2).
Edema and erythema of the posterior aspect of the larynx has traditionally been regarded as the sine qua non of
reflux laryngitis. This region of the larynx is in close proximity to the esophageal inlet, and is in a reflux-dependent
position when supine. Hypertrophy of the posterior
commissure is graded as mild when there is a mustachelike appearance of the posterior commissure mucosa, and
moderate when the posterior commissure mucosa is
swollen enough to create a straight line across the back of
the larynx. Posterior commissure hypertrophy is severe
when there is bulging of the posterior larynx into the
airway, and obstructing when a significant portion of the
airway is obliterated. It is important to emphasize, however, that the posterior aspect of the glottis makes up only
a small portion of the entire larynx. Preliminary studies
suggest that the epithelial defense mechanisms of the posterior commissure may differ from other parts of the larynx.7 This area may demonstrate greater resistance to injury caused by exposure to acid and activated pepsin,
which may also explain the paucity of laryngeal carcinoma observed in this region. Further, inflammation of
this region alone is unlikely to cause hoarseness. Thus,
evaluation of the entire larynx is necessary when assessing
reflux-induced tissue injury.
In 1995, Koufman8 first described pseudosulcus vocalis,
a pattern of edema on the ventral surface of the vocal fold
that extends from the anterior commissure to the posterior
larynx. Also called infraglottic edema, pseudosulcus can be
differentiated from sulcus vergeture, which is caused by adherence of the vocal fold epithelium to the vocal ligament
secondary to the absence of the superficial layer of lamina
propria. Although true sulcus stops at the vocal process and
is in the mid-portion of the vocal fold striking zone,
pseudosulcus extends all the way to the back of the larynx
(Figure 3). Hickson et al.9 reported that the finding of
pseudosulcus had a positive predictive value for LPR of 90%.
Heman-Ackah et al.10 reported an association between inferior glottic ridges that prevent vocal fold closure and LPR
in 2 patients with dysphonia. Using an asymptomatic control group, we reported the sensitivity and specificity of
pseudosulcus to be 70% and 77%, respectively, for the diagnosis of pH-documented LPR.11 Thus, the presence of
pseudosulcus alone is suggestive of a diagnosis of LPR. Its
presence contributes 2 points to the RFS.
Vocal fold granulomas are benign but highly recurrent
lesions that typically occur on the vocal process of the aryte-

noid cartilage (Figure 4). Histologically, they consist of hyperplastic squamous epithelium with proliferated fibroblasts, capillaries, collagen fibers, and leukocytes.12,13 These
lesions were once thought to occur as a result of excessive
mechanical trauma on the vocal process as may occur with
hyperkinetic laryngeal behavior, chronic cough, endotracheal intubation, and excessive throat clearing. The recent
otolaryngologic literature, however, implicates LPR as an
important etiologic factor.12,14 16
The Waldeyer ring is a circle of lymphatic tissue
formed by the 2 palatine tonsils, the pharyngeal tonsil, the
lingual tonsil, and intervening lymphoid tissue. An association between hypertrophy of Waldeyer ring lymphatics and extraesophageal reflux has recently been suggested. Mamede et al.17 reported lymphoid hypertrophy
of the base of the tongue (lingual tonsils) in 62% of persons with laryngoscopic signs of reflux and in 75% of
persons with pharyngolaryngeal symptoms of LPR. Carr
et al.18 reported hypopharyngeal cobblestoning in 3% of
children with gastroesophageal reflux disease.18 We have
coined the term reflux pharyngitis to refer to lymphoid
hypertrophy of the posterior pharyngeal wall (Figure 5).
Lymphoid hypertrophy of the Waldeyer ring may also be
associated with various other pathologic entities such as
infection and neoplasm. One must keep a high index of
suspicion for alternative causes of lymphoid hypertrophy. Nonetheless, the association between lymphoid hypertrophy and reflux appears to be genuine.
Excessive throat mucus is another endoscopic finding
that may be attributed to LPR. The so-called water
brash is defined as the sudden filling of the mouth with
clear mucus. Water brash is associated with the occurrence of heartburn. The salivary bicarbonate released
during a reflux episode is thought to act as an endogenous
antacid that serves as a protective response to neutralize
stomach acid.19 The sensation of excessive throat mucus
associated with water brash may be confused with the
sensation of postnasal drip and the diagnosis of rhinitis.
Differentiating between water brash and postnasal drip
syndrome may at times be difficult. An alternating therapeutic and diagnostic trial with medication aimed at allergic rhinitis and LPR may help distinguish between the
2 causative factors.

SUMMARY
The diagnosis of LPR can, at times, be elusive. The disorder can be intermittent. LPR symptoms are nonspecific
and not always associated with endoscopic findings, and
hypopharyngeal reflux occurs to some extent in asymptomatic individuals. Thus, the clinician must use various
modalities to arrive at a diagnosis. A thorough understanding of endoscopic pharyngeal and laryngeal findings
and their relation to patient symptoms is essential to suc-

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Figure 3. Bilateral pseudosulcus vocalis. Also present is moderate posterior commissure hypertrophy.

Figure 4. Granuloma on the vocal process of the left vocal fold.

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Figure 5. Lymphoid hypertrophy of posterior pharyngeal wall, also referred to as cobblestoning or reflux pharyngitis.

cessfully diagnose and treat patients with LPR. The RFS

may provide a useful framework for describing refluxinduced laryngeal tissue injury.

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