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Gastro-esophageal Reflux Gastro-esophageal Reflux In Obstructive Sleep In Obstructive Sleep
ApneaApnea
Gastro-esophageal Reflux Gastro-esophageal Reflux In Obstructive Sleep In Obstructive Sleep
ApneaApnea
ByByAhmad YounisAhmad Younis
Professor of Thoracic MedicineProfessor of Thoracic MedicineMansoura Faculty of MedicineMansoura Faculty of Medicine
Ahmad YounisAhmad YounisProfessor of Thoracic MedicineProfessor of Thoracic MedicineMansoura Faculty of MedicineMansoura Faculty of Medicine
A condition in which the stomach contents (food or liquid) leak backwards from the stomach into the esophagus.
This action can irritate the esophagus, causing heartburn and other symptoms.
Once food is in the stomach, a ring of muscle fibers prevents food from moving backward into the esophagus. These muscle fibers are
called the lower esophageal sphincter. If this sphincter muscle doesn't close well, food, liquid, and stomach acid can leak back into the
esophagus .
Gastroesophageal reflux disease (GERD)
Biopsy
Assessment of growth
Not only can stomach acid in the esophagus cause heartburn, but it can also cause ulcers, strictures of the esophagus, hoarseness, chronic
pulmonary disease, and Barrett's esophagus (a change in the lining of the esophagus that increases the risk of
developing cancer of the esophagus).
•
Upper esophageal sphincter
•The upper esophageal sphincter (UES) is a bundle of muscles at the top of the esophagus. The muscles of the UES are under conscious control, used when breathing, eating, belching, and vomiting. They keep food and secretions from going down
the windpipe.
The aim of this work The aim of this work
was to assess the frequency of GERD in patient with OSAS was to assess the frequency of GERD in patient with OSAS
and to assess the relationship of severity of GERD to the and to assess the relationship of severity of GERD to the
severity of OSAS.severity of OSAS.
Patients and methods:Patients and methods: This study included This study included 30 OSAS30 OSAS
patients and patients and 20 controls20 controls. The patients and controls were . The patients and controls were
subjected to the following. thorough history taking, with subjected to the following. thorough history taking, with
stress on symptoms of GERD, symptoms of OSAS, stress on symptoms of GERD, symptoms of OSAS,
clinical examination, chest x-ray and full-night clinical examination, chest x-ray and full-night
polysomnography and 24 hour pH monitoring.polysomnography and 24 hour pH monitoring. ..
Table (1): Demographic data of patients with OSAS versus Controls
Patients with OSA (n
= 30)Controls
)n = 20(Statistics
Mean age56.2 ± 3.4855.5 ± 2.14t = 0.803P = 0.426
Mean BMI31.10 ± 1.1330.49 ± 1.39t = 1.701P = 0.095
Sex MaleFemale
18) 60%(12) 40%(
14) 70%(6) 30%(
2 = 0.521P = 0.470
Table (2): GERD symptoms in patients with OSAS versus Controls
Patients with OSAS (n = 30)
Controls (n = 20)Statistics
No%No%
Heart burn18604202 = 7.792P = 0.005
Regurgitation1136.72102 = 4.435P = 0.035
Dysphagia310002 = 2.128P = 0.145
Table (3): Variables of 24 hours pH monitoring in patients with OSAS versus controls
Patients with
OSAS (n = 30)Controls (n = 20)Statistics
time pH < 4 in supine position %2) 0.8 – 18(1) 0.2 – 10(U = 154.0P = 0.003
time pH < 4 in upright position %2.5) 0 – 7(0.55) 0 – 4(U = 169.0P = 0.009
Total % time pH < 42) 0.7 – 10.9(1) 0.2 – 6.2(U = 169.5P = 0.009
Number of episodes (pH < 4)41) 10 – 172(29) 7 – 172(U = 182.5P = 0.019
Number of episodes > 5 min1) 0 – 8(0) 0 – 1(U = 176.
P = 0.009
Longest episode6) 1 – 32(2.5) 1 – 7(U = 164.0P = 0.007
Demeester score10.55) 3.7 – 68(6) 1 – 29(U = 168.0P = 0.009
Table (4): Frequency of GERD in patients with OSAS versus Controls
Patients with OSAS (n = 30)
Controls )n = 20(Statistics
No%No%
GERD (De Me Master score > 14.72)
12402102 = 5.357P = 0.021 Without GERD (De
Master score < 14.72)18601890
Table (5): GERD symptoms in OSAS patients with GERD versus OSAS patients without GERD
OSAS Patients with GERD
)n = 12(
OSAS Patients without GERD
)n = 18(Statistics
N%N%
Heart burn12100633.32 = 13.333P < 0.001
Regurgitation975002 = 19.286P < 0.001
Dysphagia216.715.62 = 0.988P = 0.320
Multiple investigators noted the validity of establishing GERD on the basis of symptoms . Otolaryngol Head Neck Surg 2006; 135: 253-7.
•clinician typically diagnose and treat patients with GERD on just clinical ground, so in certain clinical situation, it can obviate the need for 24 hour PH monitoring. Aliment Pharmacol Ther; 2005; 21(9): 1127-33.
Table (6): OSA symptoms in OSAS patients with GERD versus OSAS patients without GERD
OSAS Patients with GERD
)n = 12(
OSAS Patients without GERD
)n = 18(Statistics
N%N%
Snoring121001266.72 = 5.00P = 0.025
Excessive daytime sleepiness121009502 = 8.571P = 0.003
Morning headache650316.72 = 3.810P = 0.051
Nocturnal chocking975633.32 = 5.00P = 0.025
Witnessed apnea650633.32 = 0.833P = 0.361
possible positive feedback effect of GERD on the pathophysiology of OSAS
•Arousals caused by reflux may increase daytime somnolence
•close connection between severity of GERD and score of Epworth sleepiness scale as an
indicator of daytime somnolence .
•proton pump inhibitor will markedly improve symptoms of sleepiness and reflux symptoms in patients with documented OSAS. Laryngoscope 2004; 114: 1525-28.
Table (7): Variables of polysomnography in OSAS patients with GERD versus OSAS patients
without GERD
OSAS Patients with
GERD)n = 12(
OSAS Patients without GERD
)n = 18(Statistics
Sleep efficiency89.92 ± 1.5195.39 ± 1.91t = 8.321P < 0.001
AHI37.58 ± 4.0633.50 ± 5.23t = 2.403P = 0.023
Arousal index24.25 ± 3.7714.89 ± 3.72t = 6.713P < 0.001
Desaturation index19.08 ± 1.3110.78 ± 1.52t = 15.481P < 0.001
Average SaO2 < 90%25.25 ± 3.5714.56 ± 3.87t = 7.643P < 0.001
total time SaO2 < 90% %3.54 ± 0.491.20 ± 0.62t = 11.561P < 0.001
time in snoring %18.50 ± 0.907.50 ± 5.31t = 8.611P < 0.001
•Repeated reflux causes tissue swelling and this contribute to further airway obstruction with subsequent snoring and nocturnal choking. So GERD and OSAS adversely affect the symptoms and severity of the co-
morbid condition .
•GER may result in anamnestic short awakenings that lead to sleep fragmentation and feeling un-refreshed the next morning, dozing off and daytime sleepiness . Gastroenterology 2003; 124: A-414
The AHI in OSAS patients with GERD was significant higher than OSAS patients without
GERD •This signify that the positive feedback of
GER on the pathogenesis of OSAS may occur by causing edema of the upper airway by the acidic reflux with subsequent more
AHI .
Table (8): Correlation of severity of OSAS, severity of arousal index and severity of
percentage total sleep time SaO2 < 90% to severity of GERD
Severity of GERD (De Mesteer Score)
rP
Severity of OSAS (AHI)0.3290.076
Severity of arousal index0.785 >0.001
Severity of % TST SoaO2 < 90%0.901 >0.001
Arousal index and subsequent decrease in sleep efficiency may be implicated in the pathogenesis of GERD
•This was in accordance to Kerr et al who reported that arousals may trigger GERD by causing transient alteration in the pressure gradient across the lower esophageal sphincter. Chest 1992; 101: 1539-44.
•GER occurs most commonly during the brief stages of arousals
•arousals precede transient lower esophageal sphincter relaxation
The possible role of hypoxemia in the pathogenesis of GERD
• .This was in accordance of Termato et al who reported increased GER episodes during hypoxia due to an impaired swallowing function. Chest 1999; 116, 17-
21 .
The severity of OSAS (AHI) showed no significant correlation with severity of GERD
(De Mesteer Score) •Morse et al reported that, objective
correlation between OSA and GERD which may suggest that both are common entities sharing similar risk factors but may not to be causally linked. Clin Gastro-enterol Hepatol 2004; 2: 761-768.
•When acidification of the lower esophagus occur in patients with OSA, it is probably caused by a combination of increased transdiaphragmatic pressure gradient and coexisting pathology of lower esophageal sphincter causing incomplete closure .
•GER is not caused by OSA but may be facilitated by it provided that there is already abnormal pathology in the lower esophageal sphincter
severity of OSA which is defined as higher score of AHI, does not reflect the magnitude of respiratory effort during obstruction
• .Also the upper airway resistance syndrome which is associated with respiratory effort is not included in the AHI, therefore it is not easy to conclude that the occurrence of GER is related to the number of AHI rather than the respiratory effort during each breathing cessation period. Beside the respiratory effort, repetitive stimulation of lower esophageal sphincter via phreno-esophageal ligament may also be linked with a threshold value of respiratory effort.
Conclusion: We can conclude from this study
that GERD occur more common in OSAS
patients as compared to controls (40% versus
10%) . There were significantly positive
correlation between arousal index and hypoxemic
index with severity of GERD (DeMeesre score )
while no correlation exist between severity of
OSAS (AHI) and severity of GERD (DeMeesre
score ).
Recommedation
It is recommended for sleep specialist to inquire about
GERD symptoms in patients with OSAS as it is a
common problem .
Also gastroenterologists must inquire about OSAS
symptoms in patients with GERD especially those not
responding to proton pump inhibitor .
من” الله ولينصرنينصره “
نصر” علينا حقا وكانالمؤمنين “
الله الله جزاكـــم جزاكـــم
خيــــــــراخيــــــــرا