Department of Otolaryngology, Freeman Hospital, Newcastle upon Tyne NE7 7DN, UK
Correspondence to: Mr P D Karkos E-mail: pkarkos{at}aol.com
| INTRODUCTION |
|---|
|
|
|---|
| MECHANISM OF REFLUX IN THE UPPER AERODIGESTIVE TRACT |
|---|
|
|
|---|
In a study reported last year by Tasker et al.,4 pepsin was found in middle-ear effusions of childrenan observation that generated an entirely new theory on the pathogenesis of glue ear in children. Current research focuses on developing a diagnostic tool that will identify and localize pepsin in airways tissues.
| EPIDEMIOLOGY OF REFLUX |
|---|
|
|
|---|
| EXTRA-OESOPHAGEAL MANIFESTATIONS OF REFLUX |
|---|
|
|
|---|
Reflux laryngitis
The term reflux laryngitis (or posterior laryngitis) signifies erythematous
arytenoids, a greyish appearance of the interarytenoid region, or a
combination of the two. Often this finding is accompanied by oedema. Wiener
et al. found a decrease in oesophagcal pH in 65% of patients with
chronic hoarseness and suggestive laryngeal lesions, though reflux
oesophagitis was demonstrable endoscopically in only
28%.8 Long-standing
GORD is believed to contribute to the development of laryngeal cancer; chronic
irritation of the laryngeal mucosa is thought to be a carcinogenic
factor.9
Contact granulomas
Contact granulomas appear in the area of vocal process in the posterior
third of the larynx. Voice abuse/misuse is mainly to blame, but there is
evidence that reflux
contributes.9 A
combination of proton pump inhibitor and speech therapy is the treatment of
choice rather than surgical
removal.10
Reinke's oedema
This is bilateral oedema of the subepithelial space of the vocal cords,
mostly found in elderly female smokers. Again, GORD may be a cofactor.
Treatment consists of microsurgical removal of the oedematous mucosa.
Postoperatively, proton pump inhibitors can be used together with cessation of
smoking and speech
therapy.10 If the
patient continues to smoke postoperatively, the quality of the voice will be
poor and many surgeons decline to operate unless the patient stops
smoking.
Subglottic laryngeal stenosis
Bain et al. in 1983 reported a patient with GORD, without any
history of trauma, intubation or surgery, who had developed subglottic
laryngeal
stenosis.11 After
laryngeal reconstruction of the airways and Nissen fundoplication the
condition did not recur. Subglottic stenosis has been linked to reflux in
children as well as
adults.12,13
Koufman, with pH-metry, demonstrated reflux in 24 (75%) of 32 patients with
this condition.14
The combination of GORD and laryngeal trauma (including iatrogenic injuries
such as intubation) creates the ideal environment for development of
subglottic stenosis.
Postnasal drip
Only 20% of GORD patients describe heartburn or retrosternal pain. One of
the atypical symptoms is postnasal drip, also known as catarrh, though clearly
this can have other reasons. There is much confusion about the origin of this
reflux symptom. Many patients are convinced that the annoying mucus originates
from the nose or the paranasal sinuses but in most cases there is no evident
disease in these sites. In a study of 250 patients with reflux and without any
paranasal sinus disease, postnasal drip was present in more than
three-quarters (Issing WJ, unpublished). A possible mechanism is
reflux-related damage to the ciliated epithelium of the posterior larynx and
pharynx, leading to disruption of tracheal clearance; the patient gets the
feeling of constant secretions and keeps clearing the throat. Only mild damage
to the epithelium is enough, and this explains why postnasal drip is an early
manifestation of GORD. However, postnasal drip is a vague and common symptom,
and treatment of underlying GORD may be long
delayed.15
Otolaryngologists and general practitioners usually prescribe decongestant
nasal sprays. In cases where symptoms persist for months, proton pump
inhibitors may prove useful.
Globus pharyngeus
The most common symptom reported by patients with laryngopharyngeal reflux
is a lump in the throat (globus pharyngeus). As early as 1969 Malcomson found
a link between reflux and globus pharyngeus. With the aid of barium studies he
was able to demonstrate hiatus hernia with reflux in 63% of 307 patients with
globus sensation. Subsequent studies gave conflicting
results.16
Koufman14 reported
a decrease in oesophageal pH in 16 (58%) of 27 patients, whereas Wilson et
al. found this to be the case in only 20 (23%) of 87 globus
patients.17 Hill
et al. found no difference in psychological state between patients
with globus and a control group. They reported GORD in 31% of
patients.18
Overall, it is still unclear whether reflux contributes to the aetiology of
globus. The coexistence of globus and reflux does not mean that reflux is the
cause.19
GORD and teeth
The ill-effects of gastric juice on tooth enamel have been known for many
years. Conditions such as anorexia nervosa, bulimia, vomiting of pregnancy,
chronic vomiting, alcoholic gastritis, and hiatus hernia have long been linked
with tooth erosion. Schroder et al. found that 55% of patients with
GORD had typical changes in teeth, compared with 10% of a control
group.20
GORD and the airway
Up to 60% of patients with asthma have GORD and two theories exist for the
association. According to the first, reflux generates bronchoconstriction by
stimulation of vagal reflexes. The second proposes that the
bronchoconstriction is due to microaspiration of gastric juices, worsened by
the widely used anti-asthma drug theophylline. May et
al.21 showed
that theophylline increases both gastro-oesophageal reflux and reflux-related
dyspnoea. This could be explained by the muscle-relaxant effect of
theophylline on the lower oesophageal sphincter. In
children,22
microaspiration might sometimes account for apnoea, laryngospasm, croup and
even sudden infant death syndrome. Reflex bronchoconstriction
posing as a defence mechanism is of central importance here.
Non-cardiac chest pain
The possibility of reflux should be considered in cases of atypical angina
pectoris with normal electrocardiogram or normal coronary angiogram. In a
study of 108 patients with atypical chest pain, 12 were found to have
gastrointestinal causes for their
pain,23 and in
other studies24
25-50% of patients with pain of non-cardiac origin proved to have GORD.
Differential diagnosis is difficult because the incidence of both GORD and
coronary artery disease rises with age and body inactivity and these
conditions may coexist and influence each other. For example, GORD can cause a
drop in blood pressure and a rise in heart rate, which in turn may lead to
angina pectoris and electrocardiographic changes.
Reflux and carcinoma of the upper aerodigestive tract
Only a few years ago reflux was judged trivial and not a real disease.
Today we recognize the hazard of
carcinogenesis.2
Almost 5% of patients with laryngeal cancer are nonsmokers, and reflux is
suspected of being the main factor in this group. Both tobacco smoke and
alcohol increase acid reflux, so these may interact in smokers and drinkers.
Among patients with various otolaryngological disorders the highest prevalence
of reflux was in those with
carcinoma.14
However, the exact relation between reflux and carcinoma remains unclear.
| TREATMENT |
|---|
|
|
|---|
Since motility disorders are crucial in GORD, prokinetic drugs might seem the best approach. One such was cisapride, which along with metoclopramide and domperidone gave convincing results. As well as the motility effect, it increased production of saliva and bicarbonate.25 However, this agent has cardiac side-effects. and is no longer used. At present proton pump inhibitors are the treatment of choice for laryngopharyngeal reflux, primarily because of their prophylactic effect. They act on parietal cells when pH is less than 4 and irreversibly inactivate H+/K+ ATPase.26 Lengthy step-up regimens with increasing doses of drugs are no longer used for laryngopharyngeal reflux, mainly because of the delay in healing and the high costs. More effective and cost-effective is step-down therapy, whereby the patient starts on a high dose of proton pump inhibitor such as esomeprazole 40 mg daily for 8 weeks and twice daily for non-responders.27 The standard GORD dose and duration is not adequate in laryngopharyngeal reflux and many patients relapse when treatment stops.28 The argument for twice-daily dosing is that none of the proton pump inhibitors suppresses acid for more than 17 hours.29 Treatment should continue for six months or longer, with regular review to monitor response and adjust dosage.
Anti-reflux surgery, such as Nissen fundoplication,30 is indicated in selected patients whose symptoms persist despite medication for at least a year. The case for surgery is strongest in those with typical reflux that is not improved by proton pump inhibitors and those with an associated hiatus hernia. Long-term follow-up shows no advantages for open fundoplication over use of proton pump inhibitors. For laparoscopic fundoplication the evidence does not yet exist.
| REFERENCES |
|---|
|
|
|---|
This article has been cited by other articles:
![]() |
P. Duffey Atypical manifestations of gastrooesophageal reflux J R Soc Med, February 1, 2004; 97(2): 99 - 99. [Full Text] [PDF] |
||||
![]() |
S V. Karthik Gastro-oesophageal reflux J R Soc Med, January 1, 2004; 97(1): 49 - 49. [Full Text] [PDF] |
||||
![]() |
J. Martin Gastro-oesophageal reflux J R Soc Med, January 1, 2004; 97(1): 49 - 50. [Full Text] [PDF] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||