2. Gastro-esophageal Reflux In Obstructive Sleep Apnea Gastro-esophageal Reflux In Obstructive Sleep Apnea By Ahmad Younis Professor of Thoracic Medicine Mansoura Faculty of Medicine Ahmad Younis Professor of Thoracic Medicine Mansoura Faculty of Medicine

3. 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 )

6. Biopsy

7. Assessment of growth

8. 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).ulcers

12. 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.

14. The aim of this work was to assess the frequency of GERD in patient with OSAS and to assess the relationship of severity of GERD to the severity of OSAS. was to assess the frequency of GERD in patient with OSAS and to assess the relationship of severity of GERD to the severity of OSAS.

15. Patients and methods: This study included 30 OSAS patients and 20 controls. The patients and controls were subjected to the following. thorough history taking, with stress on symptoms of GERD, symptoms of OSAS, clinical examination, chest x-ray and full-night polysomnography and 24 hour pH monitoring.. Patients and methods: This study included 30 OSAS patients and 20 controls. The patients and controls were subjected to the following. thorough history taking, with stress on symptoms of GERD, symptoms of OSAS, clinical examination, chest x-ray and full-night polysomnography and 24 hour pH monitoring..

16. Table (1): Demographic data of patients with OSAS versus Controls Statistics Controls (n = 20) Patients with OSA (n = 30) t = 0.803 P = 0.426 55.5 ± 2.1456.2 ± 3.48Mean age t = 1.701 P = 0.095 30.49 ± 1.3931.10 ± 1.13Mean BMI  2 = 0.521 P = 0.470 14 (70%) 6 (30%) 18 (60%) 12 (40%) Sex Male Female

17. Table (2): GERD symptoms in patients with OSAS versus Controls Statistics Controls (n = 20) Patients with OSAS (n = 30) %No%  2 = 7.792 P = 0.005 2046018Heart burn  2 = 4.435 P = 0.035 10236.711Regurgitation  2 = 2.128 P = 0.145 00103Dysphagia

18. Table (3): Variables of 24 hours pH monitoring in patients with OSAS versus controls StatisticsControls (n = 20) Patients with OSAS (n = 30) U = 154.0 P = 0.003 1 (0.2 – 10)2 (0.8 – 18)time pH < 4 in supine position % U = 169.0 P = 0.009 0.55 (0 – 4)2.5 (0 – 7)time pH < 4 in upright position % U = 169.5 P = 0.009 1 (0.2 – 6.2)2 (0.7 – 10.9)Total % time pH < 4 U = 182.5 P = 0.019 29 (7 – 172)41 (10 – 172)Number of episodes (pH < 4) U = 176. P = 0.009 0 (0 – 1)1 (0 – 8)Number of episodes > 5 min U = 164.0 P = 0.007 2.5 (1 – 7)6 (1 – 32)Longest episode U = 168.0 P = 0.009 6 (1 – 29)10.55 (3.7 – 68)Demeester score

19. Table (4): Frequency of GERD in patients with OSAS versus Controls Statistics Controls (n = 20) Patients with OSAS (n = 30) %No%  2 = 5.357 P = 0.021 1024012 GERD (De Me Master score > 14.72) 90186018 Without GERD (De Master score < 14.72)

20. Table (5): GERD symptoms in OSAS patients with GERD versus OSAS patients without GERD Statistics OSAS Patients without GERD (n = 18) OSAS Patients with GERD (n = 12) %N%N  2 = 13.333 P < 0.001 33.3610012Heart burn  2 = 19.286 P < 0.001 00759Regurgitation  2 = 0.988 P = 0.320 5.6116.72Dysphagia

21. 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.

22. Table (6): OSA symptoms in OSAS patients with GERD versus OSAS patients without GERD Statistics OSAS Patients without GERD (n = 18) OSAS Patients with GERD (n = 12) %N%N  2 = 5.00 P = 0.025 66.71210012Snoring  2 = 8.571 P = 0.003 50910012Excessive daytime sleepiness  2 = 3.810 P = 0.051 16.73506Morning headache  2 = 5.00 P = 0.025 33.36759Nocturnal chocking  2 = 0.833 P = 0.361 33.36506Witnessed apnea

23. 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.

24. Table (7): Variables of polysomnography in OSAS patients with GERD versus OSAS patients without GERD Statistics OSAS Patients without GERD (n = 18) OSAS Patients with GERD (n = 12) t = 8.321 P < 0.001 95.39 ± 1.9189.92 ± 1.51Sleep efficiency t = 2.403 P = 0.023 33.50 ± 5.2337.58 ± 4.06AHI t = 6.713 P < 0.001 14.89 ± 3.7224.25 ± 3.77Arousal index t = 15.481 P < 0.001 10.78 ± 1.5219.08 ± 1.31Desaturation index t = 7.643 P < 0.001 14.56 ± 3.8725.25 ± 3.57Average SaO2 < 90% t = 11.561 P < 0.001 1.20 ± 0.623.54 ± 0.49total time SaO2 < 90% % t = 8.611 P < 0.001 7.50 ± 5.3118.50 ± 0.90time in snoring %

25. . 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

26. 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.

27. 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) Pr 0.0760.329Severity of OSAS (AHI) < 0.0010.785Severity of arousal index < 0.0010.901 Severity of % TST SoaO2 < 90%

28. 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

29. 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.

30. 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.

31. 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

32. 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.

34. 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 ).

35. 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.

36. ” ولينصرن الله من ينصره “ ” وكان حقا علينا نصر المؤمنين “

37. جزاكـــم الله خيــــــــرا