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AerophagiaSleepReview

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NEWS

Aerophagia
Published on October 2, 2010
Aerophagia (from the Greek aerophagein meaning to eat air) is the excessive swallowing of air. If an
excessive amount of air reaches the stomach, abdominal distension, belching, and flatulence can result.
After beginning continuous positive airway pressure (CPAP) treatment, some people struggle with these
symptoms, causing them to discontinue the therapy. Scientists have long suspected that CPAP
treatment, especially at high pressures, results in aerophagia by forcing excessive amounts of air
through the esophagus into the stomach. However, recent studies indicate that the problem may not be
related to the pressure, but to impaired function of the esophageal sphincters.

BACKGROUND
The esophagus is a long tubular organ that extends from the lower pharynx to the stomach. A tonically
contracted ringlike band of muscle fibers (sphincter) is located at each end of the esophagus. The upper
esophageal sphincter (UES) is located at the junction of the pharynx and esophagus, and the lower
esophageal sphincter (LES) is located at the lower end of the esophagus just before it enters the
stomach. On swallowing, the UES reflexively relaxes, allowing the food to enter the esophagus. A few
seconds after swallowing, the LES also relaxes and remains open for 5 to 8 minutes. After food has passed through the UES,
sequential muscle contractions (primary peristalsis) propel the food down the esophagus toward the stomach. Since the LES is
relaxed, the food then enters the stomach. If primary peristalsis does not fully clear the esophagus, the presence of any residual food
triggers secondary peristalsis (peristalsis that is not preceded by a swallow).1 The UES and LES ultimately resume their tonic
contraction. With the LES contracted, food can not flow back from the stomach into the esophagus.
NEWS
PRODUCTS
BUYER'S GUIDE
RESOURCES
Up to 30 ml of air is normally swallowed with food.2 The stomach distends as the air ingested with each swallow exerts increasing


DIGITAL
EDITION
pressure
within
it. Once the pressure reaches a certain
the LES reflexively relaxes. This allows the air to escape
27 point
0 in the stomach,
2
out of the stomach, up the esophagus, and out of the mouth as a belch.

CPAP-RELATED AEROPHAGIA

For some people treated with CPAP, arousals from sleep due to frequent belching or other symptoms of aerophagia can be
problematic. Although not all CPAP users struggle with aerophagia symptoms, the prevalence of aerophagia in people using CPAP is
unknown. One study,3 however, found a 13% prevalence of aerophagia in patients with chronic respiratory failure who were being
treated with noninvasive intermittent positive airway pressure (bi-level positive airway pressure [BPAP] or by a portable volume
ventilator).
Why only some CPAP users struggle with aerophagia symptoms perplexes scientists. One reason for the uncertainty is that it is
unclear to what extent the pressure used in CPAP treatment is truly forcing air into the stomach.2 It may be that some CPAP users
complaining of aerophagia have supragastric aerophagia in which air enters the esophagus but does not reach the stomach. Belching
can be a symptom of supragastric aerophagia, as well as gastric aerophagia in which the excess air would reach the stomach. A
second reason for the uncertainty is that studies have not proven that there is a higher prevalence of aerophagia in CPAP users whose
therapeutic pressure is high,2 which would be expected if the pressurized air were being forced through the UES and LES into the
stomach.
With the hypothesis that CPAP-related aerophagia may involve excessive amounts of air passing through the LES and noting
gastroesophageal reflux disease (GERD) involves improper functioning of the LES, a recent study by Watson and Mystkowski1
investigated whether CPAP-related aerophagia could be associated with the presence of GERD. In people with GERD, transient
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relaxations of the LES allow gastric juices to reflux from the stomach into the esophagus. The consequences can be pain, heartburn,
esophageal erosion, andif the gastric juices reach the larynxhoarseness and coughing.
In their study, Watson and Mystkowski compared the prevalence of GERD in 22 CPAP users who reported symptoms of aerophagia
versus its prevalence in 22 CPAP users who did not report symptoms of aerophagia. All of the study participants had sleep-disordered
breathing (SDB, defined as an apnea-hypopnea index greater than 10 events/hour) and the presence of other SDB symptoms such as
snoring, excessive daytime sleepiness, witnessed apneas, and morning headaches. They found a higher prevalence of GERD
symptoms in the aerophagia group than in the control group (77.3% vs 36.4%, respectively) and a greater use of GERD medications in
the aerophagia group than in the control group (45.5% vs 18.2%, respectively). From this, the researchers concluded that CPAP-related
aerophagia may be more related to the presence of GERD (since dysfunction of the LES could allow excessive amounts of air to enter
the stomach) and to the use of GERD medications (since some GERD medications impact the tone of the LES).
Studies on premature infants could potentially provide more insight into the causes of CPAP-related aerophagia. CPAP treatment is
used in neonatal intensive care units to help premature infants breathe; it also reduces the need for intubation and surfactant use.4
However, common consequences of CPAP treatment in premature infants are CPAP belly (extensive abdominal distension), and
CPAP neck (distension of the upper esophagus and lower pharynx due to the presence of excessive air).
Scientists are not sure why CPAP belly and CPAP neck occur in premature infants, but some speculations are that CPAP belly may
result from decreased or lack of bowel motility,5 that CPAP neck may result if the UES is closed or if the UES is open while the LES
remains closed,4 and that both CPAP belly and CPAP neck may be the result of decreased tone of the pharyngeal muscles.4
Differences in the function of esophageal sphincters in premature infants who develop CPAP belly and CPAP neck compared with
premature infants who do not develop these symptoms have not yet been extensively investigated.
Some infants who develop CPAP belly can intermittently tolerate CPAP treatment without developing abdominal distension and the
episodes of distension become less frequent as the infant matures. If abdominal distension persists, the infant may be treated with
glycerin suppositories and/or rectal stimulation.5

RELIEF AND TREATMENT

For adult CPAP users, relieving CPAP-related aerophagia may involve reducing the intraesophageal pressure on the LES (eg, by
elevating the head of the bed or by avoiding eating soon before bedtime); avoiding substances such as caffeine and nicotine that
induce the relaxation of the LES; and reducing the pressure within the airway. In the latter approach, some people find relief from
CPAP-related aerophagia by using an autotitrating CPAP machine. How autotitrating CPAP therapy reduces aerophagia in some
people is unclear.
Some studies show that esophageal responses to a stimulus can differ, depending on whether the esophagus is quickly or slowly
distended with pressure. In 2001, Lang6 and colleagues found that esophageal receptors trigger relaxation of the UES on sensing
rapid distension, but activate contraction of the upper esophagus (including contraction of the UES) on sensing slow distension. To
what extent positive airway pressure triggers slow or rapid esophageal reflexes that in turn contribute to or reduce CPAP-related
aerophagia has not been determined.

DRUG THERAPY AND SURGERY

Reducing the intraesophageal pressure on the LES, avoiding substances that induce the relaxation of the LES, and reducing airway
pressure, while helpful to some people, are minimally effective for others. Therefore, scientists have begun considering other treatment
options such as drug therapy or surgery to treat CPAP-related aerophagia. Some drugs that have been suggested are atropine,1
scopolamine,1 and baclofen,2 and a surgery that has been suggested is gastric fundoplication.1 All of these options have yet to be
investigated as a treatment for CPAP-related aerophagia.
The antimuscarinic drugs atropine and scopolamine have been used to treat GERD. The drugs reduce hydrochloric acid production by
blocking muscarinic receptors on specialized cells (parietal cells) in the stomach. Atropine also reduces secondary peristalsis. Some
scientists suspect secondary peristalsis, triggered by the pressurized air in CPAP treatment, may propel excessive air into the stomach
and result in aerophagia1; atropine would ideally reduce aerophagia by blocking this process. Scopolamine also reduces gastric
motility, which may allow it to reduce CPAP-related aerophagia.
The drug baclofen is an agonist of a receptor for the inhibitory neurotransmitter gamma-amino butyric acid (GABA). Baclofen inhibits
the ability of mechanoreceptors in the stomach to send signals toward the brain. Signals from the mechanoreceptors would normally
trigger transient LES relaxations. In people with GERD, this may allow the reflux of stomach acids into the esophagus. With this action
blocked by baclofen, transient LES relaxations are inhibited and the LES remains contracted. In a person with CPAP-related
aerophagia, the baclofen-induced closure of the LES would ideally inhibit excessive amounts of air from entering the stomach.
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Gastric fundoplication is a surgery that is sometimes used to treat GERD when other methods have failed. It involves wrapping the
upper part of the stomach around the LES to provide support to the LES and help it remain closed, thereby preventing the reflux of
gastric juices into the esophagus. As a possible treatment for CPAP-related aerophagia, the procedure would ideally prevent excessive
amounts of air from entering the stomach through the LES.

FURTHER RESEARCH
The results of a recent study by Bajaj7 and colleagues may be useful in future studies on CPAP-related aerophagia, although the focus
was on GERD. Bajaj measured the UES tone during different stages of sleep in 13 healthy volunteers. Bajaj found that the lowest UES
tone occurred during slow wave sleep (SWS). However, the UES tone had progressively decreased from wake to stage 2 to REM sleep.
Bajaj then measured the threshold pressure needed in different sleep stages to trigger a UES contraction followed by secondary
peristalsis. This two-part reflexive action is believed to help keep the esophagus clear of secretions, including saliva and other fluids.
Bajaj found that the reflexive action could be induced in all stages of sleep (with the possible exception of SWS) and is most easily
elicited during REM sleep. Bajajs findings could potentially be used in studies investigating the extent that different sleep stages
contribute to CPAP-related aerophagia. Studies have found that the reflex can be induced by air,7 and, as a result, some scientists
believe it may play a role in CPAP-related aerophagia.1
Many areas remain to be investigated concerning CPAP-related aerophagia, such as:
The relation between it and gastroesophageal disorders that impact LES function, including GERD and hiatal hernia1;
The extent people complaining of CPAP-related aerophagia may have asymptomatic GERD or hiatal hernia (which can be
asymptomatic and associated with gastroesophageal reflux);
The prevalence of people complaining of CPAP-related aerophagia who later develop GERD; and
Whether CPAP-related aerophagia could be associated with more severe GERD pathology.
Despite not having answers to these questions, Watson and Mystkowski suggest that patients complaining of CPAP-related
aerophagia may need to undergo esophageal evaluations.
Patients who discontinue the CPAP treatment because of aerophagia symptoms potentially risk suffering the consequences of
untreated OSA, which has been associated with cardiovascular vascular problems, increased fasting glucose levels, and lipid
abnormalities. Therefore, future studies that determine the exact causes of CPAP-related aerophagia could potentially lead to the
development of new treatments that help patients struggling with aerophagia remain on CPAP therapy.
Regina Patrick, RPSGT, is a contributing writer for Sleep Review. She can be reached at sleepreviewmag@allied360.com.

REFERENCES
1. Watson NF, Mystkowski SK. Aerophagia and gastroesophageal reflux disease in patients using continuous positive airway
pressure: a preliminary observation. J Clin Sleep Med. 2008;4(5):434438.
2. Orr WC. CPAP and things that go burp in the night. J Clin Sleep Med. 2008;4(5):439440.
3. Criner GJ, Brennan K, Travaline JM, et al. Efficacy and compliance with noninvasive positive pressure ventilation in patients
with chronic respiratory failure. Chest. 1999;116(3):667675.
4. Walor D, Berdon W, Anderson N, et al. Gaseous distention of the hypopharynx and cervical esophagus with nasal CPAP: a
mimicker of pharyngeal perforation and esophageal atresia. Pediatr Radiol. 2005;35:11961198.
5. Jaile JC, Levin T, Wung JT, et al. Benign gaseous distension of the bowel in premature infants treated with nasal continuous
airway pressure: a study of contributing factors. AJR Am J Roentgenol. 1992;158:125127.
6. Lang IM, Medda BK, Shaker R. Mechanisms of reflexes induced by esophageal distension. Am J Physiol Gastrointest Liver
Physiol. 2001;281:G1246G1263.
7. Bajaj JS, Bajaj S, Dua KS, et al. Influence of sleep stages on esophago-upper esophageal sphincter contractile reflex and
secondary esophageal peristalsis. Gastroenterology. 2006;130(1):1725.

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