Voice Articles
It’s Due to Reflux – Or is it?
Reflux causes everything – or so it often seems when we read
both scientific and lay journals and magazines on this subject.
Reflux has been implicated in causing a great variety of maladies
of the upper aerodigestive tract ranging from sinusitis to dysphagia
to cancer. What is the truth? How can we accurately diagnose and
treat reflux? In the last decade a large volume of scientific literature
has been published on these topics, but many of the answers are
anything but clear.
In this short space I hope to summarize some of our current knowledge
about laryngopharyngeal reflux and will also highlight some areas
of uncertainty.
What is reflux?
First a few definitions. Laryngopharyngeal reflux (LPR) is the
retrograde flow of gastric contents to the laryngopharynx. This
is different than gastroesophageal reflux disease (GERD) where there
are gastric contents refluxing back into the distal or mid esophagus.
GERD has been studied longer than LPR and reasonably good data exists
on how much acid exposure to the distal esophagus constitutes an
abnormal amount. GERD is frequently associated with heartburn and
can be diagnosed in a variety of ways including endoscopy and distal
pH probe testing where a standardized scoring system exists.
LPR is much more problematic. Though studies are continuing, there
is no accepted standard for the measurement of the amount of gastric
contents coming up through the upper esophageal sphincter. In GERD,
repeated exposure of the distal esophagus to a pH below 4 is considered
to be damaging. We all, however, have some distal reflux(which is
considered normal) and our distal esophagus is generally able to
tolerate some acid exposure without substantial negative impact.
With LPR, exposures to pH values below 4 are certainly damaging,
but many feel that pH values much higher than this could also be
damaging as the epithelium lining the laryngopharynx is not adequately
equipped to handle such exposures. Even relatively short exposures
of the pharynx to gastric contents could be damaging. If every short
episode of lower esophageal reflux also came all the way up into
the pharynx this could be problematic. One could therefore see how
LPR could occur in the absence of GERD.
So even though it is understood that LPR is retrograde flow into
the laryngopharynx, the exact definition of what constitutes an
abnormal amount of flow or pH of the refluxate remains unknown.
Diagnosis
History. Multiple symptoms can occur with LPR. Some of the more
common manifestations include throat irritation, chronic cough,
lump in throat sensation, and hoarseness. Belafsky et al have developed
a self-administered tool, the Reflux Symptom Index which can aid
in determining the likelyhood of LPR. (Figure 1)
Laryngeal Exam. With improvement in fiberoptic and digital technology,
very detailed exams of the larynx are easily performed. Unfortunately
exam findings are nonspecific and are those of chronic inflammation
and irritation. Major findings include posterior commissure edema,
subglottic edema, erythema, ventricular obliteration, diffuse edema,
and granuloma.(Figure 2) While some studies have shown that these
findings correlate well with documented LPR, others have shown poor
correlation and have noted these changes in a good number of individuals
without other evidence of reflux disease.
Dental Exam. We tend to focus on laryngeal findings, but dentists
have known for some time that gastric contents can damage the dentition.
In those with bulimia or with severe LPR enamel erosion can be seen
particularly on the lingual surface of the teeth. (Figure 3)
pH Probe. 24-hour pH probe monitoring can be done to provide more
information regarding the amount of laryngopharyngeal reflux occurring.
It is important that this test not be done in the standard fashion
where the probe is positioned 5cm above the lower esophageal sphincter.
This will aid in diagnosing GERD but is not helpful with LPR. When
performing a pH probe for LPR, the proximal pH sensor is typically
placed just above the upper esophageal sphincter. This is another
area of controversy as there is no well-established standardized
placement technique or scoring system. Despite these shortcomings
this is still likely the most accurate test that is widely available.
More studies are coming out where a multichannel intraluminal impedance
probe has been used to examine both acid and nonacid reflux events,
but even less standardization exists at this point.
Esophagoscopy. Esophagoscopy is often used for the diagnosis and
monitoring of complications related to GERD. This approach is not
nearly as helpful for LPR.
Specific Disease Entities
Though symptoms of LPR are often nonspecific, there are a variety
of disease entities that may be caused by or made worse by LPR.
The following is a list of these entities with a brief synopsis
of current literature regarding their association with LPR.
Sinusitis. Several studies have found that chronic rhinosinusitis
occurs more frequently in those with LPR than in those without.
Also medically refractory sinusitis has been associated with a higher
likelihood of LPR. Though is an association, it is unclear if LPR
is a coexistant disease processes or actually a cause of rhinosinusitis.
Otitis media. Studies are inconsistent. Pepsin(apparently from
the stomach) has been found in the middle ear of children with chronic
otitis media, though a clear causative relationship has not been
determined.
Postnasal drainage. It appears that LPR is one potential cause.
Postnasal drainage is extremely nonspecific and so common that other
causes also always need to be considered.
Cough/sore throat. In certain instances LPR may directly cause
a cough and sore throat. Again, these symptoms are nonspecific and
other causative factors are possible.
Irritable larynx. This diagnosis can be a bit difficult in and
of itself. At our Voice Center we do frequently see individual who
fall into this category. Typical presentations include cough, tightness,
and laryngospasm that can occur with exercise, changes in temperature
or exposure to irritants. There is little scientific data to prove
the LPR is a factor, though empiric treatment for LPR seems to help
some individuals.
Hoarseness. LPR can lead directly to hoarseness and can contribute
to formation of laryngeal granulomas. Several studies have shown
improvement in granulomas with treatment for reflux.
Dysphagia/globus. Reflux can lead to dysphagia. A globus-type sensation
in the throat is frequently associated with LPR though good studies
are lacking.
Airway stenosis. It is generally accepted that LPR can lead to
or at least contribute to the development of subglottic and tracheal
stenosis.
Cancer. Studies are not terribly definitive. LPR does not appear
to be a large risk factor for the development of laryngeal carcinoma.
Treatment
Behavioral changes. Patients should be educated on maintaining
an appropriate weight, smoking cessation and an appropriate diet.
Dietary changes would include restriction of caffeine, fats, tomato-based
products, alcohol, and late-night meals.
Medical management. Several categories of medications have been
used to treat reflux: proton pump inhibitors(PPIs), H2 – receptor
blockers, mucosal cytoprotectants, prokinetic agents, and antacids.
PPIs are the mainstay of treatment. Typically a 3 month trial is
needed to determine if the treatment is beneficial. It is important
to take these medications approximately 30 minutes prior to eating
and it should be noted that BID treatment may be necessary. Should
no significant improvement occur within 3 months, more definitive
testing such as pH monitoring should be considered.
It is not infrequent that a patient feels improvement with treatment
and yet laryngeal findings of reflux continue to persist. The significance
of this is unknown.
H2 blockers such as ranitidine may be of some benefit though are
less effective than the PPIs. Mucosal cytoprotectants and antacids
play a larger role in relief of GERD than in LPR. Prokinetic agents
have largely fallen out of favor due to various adverse reactions.
Surgery. Laparoscopic fundoplications are now fairly common and
have been shown to improve the competency of the lower esophageal
sphincter. It is not completely clear how well theses laparscopic
procedures will hold up long-term.
Conclusion
LPR is an entity that has received much attention in recent years.
While medications have improved and research has continued, accurate
diagnosis often remains elusive as symptoms and exam findings are
frequently nonspecific. We, as clinicians, should be aware of the
potential symptoms that reflux may cause and at the same time should
realize – reflux does not cause everything.
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