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Reflux Laryngitis

Bardia Amirlak, MD Assistant Professor of Plastic Surgery, Director of Residency Cosmetic
Clinic, Director of Plastic Surgery Global Health Program, University of Texas Southwestern
Medical Center at Dallas; Chief of Hand and Peripheral Nerve Surgery, Dallas Veterans
Affairs Medical Center
Bardia Amirlak, MD is a member of the following medical societies: American College of
Surgeons, American Society of Plastic Surgeons, American Society of Reconstructive
Transplantation, Kleinert Society

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 refluxrelated 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


Globus sensation

Chronic cough or throat clearing



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 management of patients with suspected laryngeal manifestations of GERD continues to
be controversial.[4] Issues are whether laryngopharyngeal reflux is a real disease, whether
laryngeal physical exam in patients with symptoms of GERD is useful as a marker for
response to treatment, how to differentiate and treat patients with chronic laryngitis with and
without reflux symptoms, and the benefits of PPIs in patients with different symptoms.
Continued acid suppression is unlikely to provide dramatic symptom improvement for
patients whose conditions are completely unresponsive after 1-2 months of treatment with
twice-daily PPI. Vaezi et al state "Any suggestions that reflux still may be playing a role in
patients refractory to therapy, especially if suggested by nonspecific laryngeal findings, is a
less than optimal use of resources and should be discouraged."[4]
The image below is a scoring system for presence and degree of symptoms.

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.[5]
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.[6] 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.

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

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).[7]
The following 4 physiological barriers protect the upper aerodigestive tract from reflux

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
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.[8]
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
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.[9]
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.[10]


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 47% 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.[11]

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.[6]
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.

No particular racial predilection reported.

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

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