gerd.pptx

GASTROESOPHAGEAL REFLUX DISEASE

1. GERD PATHOPHYSIOLOGY AND DIAGNOSIS DR SUJAN SHRESTHA MCh, Surgical Gastroenterology

2. Definition 44 experts from 18 countries Main aim of global definition and classification of GERD

3. GERD is a condition which develops when the reflux of stomach contents causes troublesome symptoms and/or complications Troublesome Mild symptoms minimum two times per week Moderate to severe symptoms at least one per week Symptoms Typical Atypical Extraesophageal symptoms Complications Esophagitis Stricture Barrett esophagus Adenocarcinoma Definition Acid reflux Nonacid reflux

4. Burden of GERD One of the Most common gastrointestinal problem Cost of GERD from direct and indirect medical costs is more than $12.1 billion per year and $515 million per year, respectively. Esophagitis Stricture Barrett esophagus Adenocarcinoma Complications

5. Burden of GERD The prevalence of GERD among Nepalese residing in Brunei Darussalam was 7.2%. If same rate is considered than around 20 – 25 lakhs Nepalese is suffered from GERD GERD might be much higher in Nepalese population where most of these patient are under over-the-counter PPI therapy. Actual prevalence requires cross sectional studies

6. Pathophysiology of GERD 2 IMPORTANT DETERMINANTS LES NATURE OF REFLUXATE

7. Pathophysiology of GERD Esophagus Stomach Low pressure zone High pressure zone Tendency for reflux as per pressure gradient High pressure door system that prevents reflux under normal condition

8. Pathophysiology of GERD High pressure door system LES Allison ligament Diaphragm Gastric cardiac muscles So, its always closed except Swallowing Burping Vomiting

9. Pathophysiology of GERD LES The LES has no clear anatomic boundaries and is not visible endoscopically, by CT scan or by endoscopic ultrasound Three important characteristics of the LES Total LES length, Intra-abdominal length, and Resting pressure. All these parameters possible via esophageal manometry

10. LES Pulling the manometer with probe up

11. Pathophysiology of GERD LES is usually closed preventing reflux LES relaxes during 2 conditions 1. Swallow DLESR : Deglutitive lower esophageal sphincter relaxation Food bolus in mouth and pharynx UES and LES to relax till the food is transferred to stomach Vagal input due to bolus

12. Pathophysiology of GERD 2. Burping TLESR :T ransient LES relaxation (TLESR) Dr. Jerry Dodds in 1982. GASTRIC DISTENTION OR NON PRESSURISED GASTRIC DILATATION Eg: heavy meal or carbonated drinks Transient relaxation of normal LES

13. Transient relaxation of normal LES How the relaxation occurs with gastric distention ? 2 theories 1. Neuromediated reflex Gastric distention Stimulate stretch receptors in the gastric fundus Stimulate vagal afferent nerve fibers Medullary nuclei Efferent limb of the reflex via the vagal and phrenic nerves Elicit TLESR, Crural diaphragm inhibition, and Distal esophageal shortening.

14. 2. Effacement or mechanical theory

15. Transient relaxation of normal LES How the relaxation occurs with gastric distention ? 2. Effacement or mechanical theory Gastric distention Effaced portion is taken up by the expanding fundus. At this length, the corresponding pressure of the LES can no longer maintain The abdominal length shorten (if less than 1 cm) LES relax TLESR

16. Transient relaxation of normal LES Abdominal length is restored after distention is over Its dynamic failure Permanent failure of LES Repeated exposure of lower esophagus to acid to repeated TLESR PERMANENT shortening of LES Permanent LES failure GERD (more severe and complications) Continued eating habits (predisposing factors)

17. “Permanent failure of the LES” When one or more of the following LES abnormalities are seen on a resting motility study performed in the fasted patient: Abdominal length of 1 cm or less, Overall length of 2 cm or less, and Resting pressure of 6 mm Hg or less Complicated GERD are associated with permanent LES failure

18. “Permanent failure of the LES” Severity of complications directly proportional to LES component's failure Stein HJ. Ann of surg 1992 More LES component failure a/w Higher pH score ( more acid reflux) More severe GERD

19. Pathophysiology of GERD 2 IMPORTANT DETERMINANTS LES NATURE OF REFLUXATE

20. Pathophysiology of GERD NATURAL HISTORY OF GERD CATEGORICAL CONCEPT Patient categorized as NERD ERD Will stay in same category SPECTRUM CONCEPT NERD ERD BARRETT ADENOCA proGERD STUDY FROM EUROPE (2721 PATIENTS) Disease progression to BE was seen in 6 % in NERD 12% in mild ERD 19% in severe ERD CONCLUSION: GERD IS PROGRESSIVE DISEASE SO HOW THE PROGRESSION OCCURS? CAN WE HALT OR AT LEAST SLOW IT DOWN? Am J Gastroenterol. 2006

21. Pathophysiology of GERD NATURE OF REFLUXATE Broadly divided into 2 Acid Nonacid ( weak acid, bile ) Kaeur et al. ann of surg 1995 Acid is noxious to esophageal mucosa but is more toxic when both acid and bile is present Ok let us remove acid by using PPI SO, WILL THAT HELP IN HALTING THE PROGRESSION OF GERD ?

22. NATURE OF REFLUXATE SO PATIENT IS ON DOUBLE DOSE PPI FOUR THINGS HAPPENS 1. PH 4 OR MORE ( HEART BURN AND REGURGITATION REDUCES) 2. PH 3-5 ( INTESTINALISATION OF CARDIAC MUCOSA) 3. PH MORE THAN 4 (ORAL BACTERIA GROW IN STOMACH AND DECONJUGATES BILE RELEASE OF MORE NOXIOUS FREE BILE ACID ) 4.Bile behavior in different PH HAPPY PATIENT HAPPY DOCTOR IMMEDIATE RESULT MOST COMMON SCENARIO BUT THE PATIENT ESOPHAGUS IS NOT HAPPY AT ALL

23. NATURE OF REFLUXATE 4.Bile behavior in different PH PH less than 2 Bile and acid gets precipitated No risk PH more than 7 Bile is soluble No risk PH 3-7 Half bile soluble Half bile insoluble (unstable bile)- time bomb Very noxious Esophageal cell At lower concentration – impairs mitochondrial function At high concentration – its cytotoxic , causes mutation NERD ERD BARRETT ADENOCA Most treated patient falls under this category

24. 2 IMPORTANT DETERMINANTS LES NATURE OF REFLUXATE PPI limited symptomatic benefit Progression of GERD can be possibly halted by preventing reflux Modification of refluxate is not an option based on provided hypothesis Summary of GERD PATHOPHYSIOLOGY

25. CLINICAL FEATURE OF GERD

26. CLINICAL FEATURE OF GERD Some concept on extraesophageal symptoms in GERD HOW COUGH OCCURS ? 2 CONCEPTS Micro aspiration of refluxate Positive acid or nonacid on BAL Xray chest with features of aspiration 2. Reflex cough Refluxate In respiratory tract Aspiration cough Refluxate Lower esophagus Mucosa (acid sensitive receptors) Vagus afferent Sensory afferent Central relay Vagal efferent (cough) (convergence of afferent) Convergence due to common eso and resp embryology PPI DOESNOT WORK PPI MIGHT REDUCES COUGH

27. DIAGNOSTIC MODALITY FOR GERD Subjective Symptoms PPI trial Most common in our scenario Most cost effective Most failure Most progression Objective 24 hrs pH monitoring MII-pH ( impedence ) endoscopy Goal standard technique

28. Ambulatory pH monitoring Evolution of pH study in reflux Reichman in 1884. Showed the presence of acid in GERD using gelatin sponge Aylwin in early 1900 Showed the presence of acid and pepsin on aspirate using esophageal tube. Bernstein and Baker Acid infusion test Appearance of symptoms on installation of weak acid on distal esophagus

29. Evolution of pH study in reflux Tuttle and Grossman (pH metry equipment) Spencer in 1969 ( prolong esophageal pH measurement) Spot test Could not differentiate physiological vs pathological reflux Non portable Patient had to get admitted a day or more for test 1974 Johnson and DeMeester 24 hr ambulatory pH monitoring

30. Know the instrument Ambulatory pH CATHETERS SENSOR Glass Monocrystalline antimony (MOST COMMON) ISFET RFERENCE ELECTRODE Internal External Wire less pH capsule BRAVO capsule Data receiver belt for both

31. Procedure Patient preparation No PPI for 7 days (with vs without PPI) No antacids for 1 day Continue same food habit vs avoid acidic food Patient has to write down the time and duration of Symptoms Mealtimes Posture change (supine or upright)

32. Procedure Delineation of LES DIRECT METHOD Use of esophageal manometer (HRM) INDIRECT METHOD Use of endoscopy (SQUAMOCOLUMNAR JUNCTION) pH ELECTRODE PLACEMENT 4 CM ABOVE THE upper part of LES 6 CM ABOVE the visible junction Patient will go with the device for 24 hrs or more Data received is interpreted

33. Interpretation of data The DeMeester Score Includes six parameters: Total percent time pH less than 4.0 Percent time pH less than 4.0 in the upright period Percent time pH less than 4.0 in the recumbent period The total number of reflux episodes The total number of reflux episodes longer than 5 minutes ; and The duration of the longest reflux episode. Total score of more than 14.7 is abnormal Symptoms association: Temporal relationship between symptoms and reflux events Symptom Index (SI) The Symptom Sensitivity Index (SSI) The Symptom Association Probability (SAP). SI greater than equal to 50%

34. NATURE OF REFLUX SO if there is non acid reflux than the pH monitoring might be false negative even though there is actual reflux 24 hr pH monitor is only positive for acid refluxate Does not fulfil our sole purpose of diagnosis of reflux (acid or nonacid) “Intraluminal impedence monitoring is only device that can achieve high sensitivity for detecting all types of reflux episode. And it should be combined with pH metry for characterization of acidic reflux” Porto Consensus Sifrim D. GUT 2004

35. NATURE OF REFLUXATE MULTICHANNEL INTRALUMINAL IMPEDANCE Shows there is reflux When combined with pH STUDY MII-pH STUDY (both acid and nonacid) PH < 4 ACIDIC REFLUX PH 4-7 WEAK ACIDIC PH >7 NON-ACIDIC Silny

36. CONCEPT OF IMPEDENCE WHAT IS IMPEDENCE? OPPOSITION TO CURRENT FLOW MATTER WITH HIGH CONDUCTIVITY (ELECTRICAL) HAS LOW OR FALL IN IMPEDENCE IMPEDENCE OF AIR/ GAS > MUSCLE TISSUE > LIQUID/REFLUXATE

37. CONCEPT OF IMPEDENCE

38. CONCEPT OF IMPEDENCE

39. CONCEPT OF IMPEDENCE

40. CONCEPT OF IMPEDENCE PROXIMAL SENSOR DISTAL SENSOR

41. CONCEPT OF IMPEDENCE PROXIMAL SENSOR DISTAL SENSOR

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