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 “

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