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  1. 1. GERD
  2. 2. Introduction • Gastroesophageal reflux (GER) – physiologic process – gastric contents move retrograde from stomach to esophagus. • GER Itself is not a disease and occurs multiple times each day without producing symptoms or mucosal damage. • Montreal consensus defines GERD as “a condition which develops when the reflux of stomach contents causes troublesome symptoms and/or complications.”
  3. 3. PATHOGENESIS An imbalance between •Defensive factors protecting the esophagus A. Antireflux barriers, B. Esophageal acid clearance, C. Tissue resistance • Aggressive factors refluxing from the stomach (gastric acidity, volume, and duodenal contents).
  4. 4. A. The antireflux mechanism includes four important components: 1) lower esophageal sphincter (LES) 2) esophageal peristalsis; 3) crural diaphragm; and 4) stomach (the reservoir).
  5. 5. 1.LES • Involves the distal 3 to 4 cm of the esophagus and at rest is tonically contracted. • Lies within the hiatus created by the right crus of the diaphragm and is anchored by the phrenoesophageal ligaments, which insert at the level of the squamocolumnar junction • The proximal portion of the LES is normally 1.5 to 2 cm above the squamocolumnar junction, whereas the distal part( 2 cm), lies within the abdominal cavity • Resting LES pressure ranges from 10 to 30 mm Hg, • pressure of 5 to 10 mm Hg is necessary to prevent GER
  6. 6. A defective LES is identified by one or more of the following characteristics: 1. average pressure of less than 6 mm Hg, 2. average overall length of 2 cm or less, and 3. average length exposed to the positive pressure environment of the abdomen (intra-abdominal length) of 1 cm or less.
  7. 7. 2. Esophageal peristalsis • Clears physiologic reflux and thus reduces contact time between the esophageal epithelium and gastric fluid. • Ineffective esophageal motility can result in an abnormal esophageal exposure to gastric juice even in individuals with a mechanically effective LES and normal gastric function
  8. 8. 3. Crural diaphragm • Provides an extrinsic component to the gastro-esophageal barrier. • It is particularly important as a protection mechanism against reflux induced by sudden increases in intraabdominal pressure. • This mechanism is disrupted by the presence of a hiatal hernia where the intrinsic LES has “migrated” proximal to the diaphragmatic pinch.
  9. 9. 4. Stomach Impaired function of the stomach such as abnormal gastric emptying may contribute to GERD by increasing intragastric pressure, distension, and LES unrolling. This may occur in patients with a • large hiatal hernia, in which the herniated stomach in the chest does not empty appropriately, • gastric outlet obstruction either from malignancy or peptic ulcer disease • diabetic gastroparesis.
  10. 10. Mechanisms of Reflux • Reflux usually occurs via 4 mechanisms: – TLESR, – Low LES pressure, – Swallow-associated LES relaxation – Straining during periods of low LES pressure
  11. 11. 1. Transient Lower Esophageal Sphincter Relaxations • The most frequent mechanism for reflux in patients with healthy sphincter pressures – Independent of swallowing – Not accompanied by esophageal peristalsis – Persist longer (>10 seconds) than swallow-induced lesrs – Accompanied by inhibition of the crural diaphragm • tLESRs account for nearly all reflux episodes in healthy subjects and 50% to 80% of episodes in GERD patients
  12. 12. 2. Hypotensive LES Pressure • by either strain-induced or free reflux. • Strain-induced reflux occurs when a relatively hypotensive LES is overcome by an abrupt increase in intra-abdominal pressure from coughing, straining, or bending over. • Free reflux is characterized by a fall in intraesophageal pH without an identifiable change in intragastric pressure, usually occurring when LES pressure is less than 5 mm Hg • usually observed in patients with end-stage scleroderma or after myotomy for achalasia
  13. 13. 3. Swallow-Induced Lower Esophageal Sphincter Relaxations • 5% to 10% of reflux episodes occur during swallow induced LESRs. • more common with a hiatal hernia. • due to the lower compliance of the EGJ in hernia patients, permitting it to open at pressures equal to or lower than intragastric pressure, thereby allowing reflux
  14. 14. Hiatus Hernia • The etiology of a hiatal hernia remains unclear. • Familial clustering of GERD suggests the possibilities of an inherited smooth muscle disorder. • Animal studies propose that reflux itself causes esophageal shortening, promoting the development of a hiatal hernia. • Other studies find an association with obesity and heavy lifting, raising the possibilities that over time, chronic intra- abdominal stressors may weaken the esophageal hiatus, causing the development of a hiatal hernia.
  15. 15. The Acid Pocket • Gastric pH is usually around 2 in the fasting state. • During meals, and for approximately 90 minutes thereafter, the pH reelevated owing to the buffering effects of the food. • Herein lies a paradox because most episodes of acid reflux occur immediately after a meal. • This paradox is explained by the identification of a zone in the gastric cardia that remains unbuffered, now referred to as the acid pocket. • This pocket is postulated to be the source of acidic refluxate and has a pH considerably lower than the distal esophagus and remainder of the stomach after a meal.
  16. 16. • In GERD patients with hiatal hernia, the acid pocket is further enlarged because of the proximal migration of the LES. • when the acid pocket is located about the diaphragm, especially in a hiatal hernia, more than 70% of the tLESRs were accompanied by acid reflux. • In contrast, less than 20% of tLESRs were accompanied by acid reflux when the acid pocket was below the diaphragm
  17. 17. B. Esophageal Acid Clearance • second tier of protection against reflux damage is esophageal acid clearance. • This phenomenon involves 2 related but separate processes: volume or bolus clearance, which is the actual removal of the reflux material from the esophagus, • acid clearance, which is the restoration of normal esophageal pH following acid exposure through titration with base from saliva and esophageal gland secretions.
  18. 18. • Gravity contributes to bolus clearance when reflux occurs in the upright position. At night when supine, this mechanism is not operative unless the head of the bed is elevated. • This important lifestyle change markedly improves acid clearance time and is most beneficial in patients with aperistalsis (e.g., with scleroderma).
  19. 19. Salivary and Esophageal Gland Secretions • Saliva is the second essential factor required for normal esophageal acid clearance. The stimulus for salivation appears to be the presence of acid in the proximal esophagus (20 cm above LES). • Decreased salivation during sleep is the reason that nocturnal reflux is associated with markedly prolonged acid clearance times. • Xerostomia is associated with prolonged esophageal acid exposure and esophagitis. • Cigarette smoking promotes GER. Originally attributed to nicotine’s effect on lowering LES pressure, cigarette smokers also have hyposalivation, leading to prolonged esophageal acid clearance time
  20. 20. Tissue resistance. • This is due to a third tier for esophageal defense. • Conceptually, tissue resistance can be subdivided into • pre-epithelial, poorly developed. There is neither a well-defined mucous layer nor buffering capacity by the surface cells to secrete bicarbonate ions into the unstirred water layer. • Epithelial -consist of structural and functional components. Structural components include the cell membranes and intercellular junctional complexes of the esophageal mucosa. This structure is a 25- to 30-cell- thick layer of nonkeratinized squamous epithelium. • Postepithelial factors, provided by the esophageal blood supply. Blood flow delivers oxygen, nutrients, and bicarbonate and removes H+ and CO2
  21. 21. Gastric Factors • Gastric Acid Secretion • Duodenogastric Reflux • Delayed Gastric Emptying
  22. 22. Environmental Risk Factors
  23. 23. Medical Conditions Associated withGastroesophageal Reflux Disease
  24. 24. The role of H. pylori infection in the pathogenesis of GERD: •There is evidence that H. pylori infection has pathogenic role in GERD. •Virulent strain (Cag A positive) has inverse relationship. •Depends on anatomical distribution of gastritis – In Asia, corpus-predominant gastritis is common, and eradication therapy in these patients may increase the risk of developing GERD. – Hp antrum-predominant gastritis has been shown to be associated with hypergastrinemia and gastric hypersecretion
  25. 25. SYMPTOMS Typical GERD symptoms- • Heartburn (ascending retrosternal burning) • Regurgitation • Dysphagia ( 30%)– It can be divided into an oropharyngeal etiology, which is characterized by difficulty transferring food out of the mouth into the esophagus, and esophageal etiology, which is characterized by the sensation of food sticking in the lower chest. • Water burshing
  26. 26. Chest pain • precipitated by meals, • occurring at night while supine, • Non-radiating, • responsive to antacid medication, • or accompanied by other symptoms such as dysphagia and/or regurgitation - should trigger an evaluation for an esophageal cause. Nocturnal GERD can lead to interruptions in sleep, leading to high rates of absenteeism from work and a reduced quality of Life.
  27. 27. Laryngeal symptoms of reflux • globus sensation, • hoarseness, • throat clearing, • Postnasal drip • Laryngeal and tracheal stenosis • Laryngospasm Pulmonary symptoms -cough -shortness of breath -wheezing -pulmonary disease like asthma , chronic bronchitis
  28. 28. Tests for Gastroesophageal Reflux Disease • GERD Questionnaires (RDQ, GERD Q) • PPI test • Manometry • Barium swallow • Endoscopy • Histology • pH monitoring (catheter based or wireless) • Intraluminal impedance-pH monitoring
  29. 29. Alarm Symptoms • Dysphagia • Early satiety • GI bleeding • Odynophagia • Vomiting • Unexplained Weight loss • Iron deficiency anemia • Choking Continual pain
  30. 30. Empirical Trial of Acid Suppression • High PPI dose (e.g., omeprazole 40 to 80 mg/day), usually given for at least 2 weeks, and a positive response was defined as at least 50% improvement in heartburn. • Using this approach, the PPI empirical trial has a sensitivity of 68% to 83% but poor specificity for determining the presence of GERD
  31. 31. Upper GI endoscopy
  32. 32. • More than 50% of patients who have typical GERD symptoms have normal endoscopic examinations. • Endoscopy are considered to be performed in patients with – Alarm symptoms (e.g. dysphagia, weight loss, bleeding, abdominal mass, age >40 years) – Diagnostic problems (e.g. atypical symptoms) – No response to empirical treatment in patient with characteristic symptoms
  33. 33. • Mild changes of GERD that may be visible to the endoscopist include mucosal erythema, edema, hyper- vascularity, friability, and blurring of the SCJ. • The best validated and most widely used classification system for reflux esophagitis now is the Los Angeles classification. • In this system, a mucosal break is defined as, “an area of slough or erythema with a discrete line of demarcation from the adjacent, more normal-looking mucosa”.
  34. 34. • Los Angeles classification. • (a) Grade A is defined as mucosal breaks confined to the mucosal fold, each no longer than 5 mm. • (b) Grade B corresponds to at least one mucosal break longer than 5 mm confined to the mucosal fold but not continuous between two folds. • (c) Grade C is characterized by mucosal breaks that are continuous between the tops of mucosal folds but not circumferential. • (d) Finally, grade D is represented by extensive mucosal breaks engaging at least 75% of the esophageal circumference.
  35. 35. Barium Esophagram It is used to • evaluate the entire anatomy of esophagus, • document the presence and size of a hiatal hernia, • stricture severity and location, • diverticula, esophageal emptying, and • the presence of gastroesophageal reflux, both spontaneously and induced by provocative maneuvers • Esophageal motility can be assessed - to some extent
  36. 36. Esophageal Manometry • Most accurate method to assess the coordination and pressure of the lower esophageal sphincter (LES) and the esophageal body. Findings in GERD- a defective LES or impaired esophageal motility. • Important component in the preoperative workup of antireflux surgery.
  37. 37. Excludes achalasia that may be occasionally misdiagnosed as GERD. • Characterizes the esophageal motility, and this information will be used to determine the surgical approach (Nissen or partial fundoplication). • Enables measurement of the precise location of the LES for accurate pH probe placement.
  38. 38. Esophageal Reflux Testing • Ambulatory intraesophageal pH monitoring is still the standard for establishing pathologic acid reflux. • Catheter based The conventional catheter-based pH monitoring system principally consists of a flexible catheter with one or more pH sensors and a data logger. • Catheter- free : wireless pH capsule • Improved patient comfort • less effect on reflux-provoking activities • fixed placement of the pH electrode (5 cm above the SCJ),
  39. 39. • Patients are encouraged to eat normally and engage in regular daily activities, with monitoring carried out for 18 to 24 hours. • Reflux episodes are defined by a pH drop of less than 4 • The percentage of total time pH is less than 4 is the most reproducible measurement for GERD ( Acid exposure time ), with reported upper limits of normal ranging from 4% to 5.5%.
  40. 40. Tracings from 48-hour esophageal pH . It is a 48-hour pH capsule study in a patient with GERD. Meals/drinksare shown by the yellow lines, supine periods are shown in blue. The orange bars represent symptoms that were associated with acid reflux.
  41. 41. MII-pH (MULTICHANNEL INTRALUMINAL IMPEDANCE-pH MONITORING) • Impedance testing measures the resistance (or impedance) to flow of a tiny current across pairs of metal electrodes implanted on a thin catheter placed transnasally in the esophagus. • Able to detect, localize, and classify reflux events as • acid, • weakly acid, or • nonacid. • The future standard for reflux detection and monitoring, especially in patients with persistent typical and/or atypical symptoms despite PPI
  42. 42. Approach to Diagnosis
  43. 43. Clinical Course • Depends to a great extent on whether the patient has erosive or nonerosive disease. • Controversy as to whether GERD exists as a spectrum of disease severity or • as a categorical disease in 3 distinct groups: erosive, nonerosive, and Barrett’s esophagus. • in follow-ups ranging from 6 months to longer than 22 years, less than 25% of patients with nonerosive disease evolved over time to having erosive esophagitis,
  44. 44. Nonerosive Disease • Endoscopy-negative GERD patients are more likely to be female, younger, thin, and without hiatal hernia, and they have a higher prevalence of functional GI disorders. • First patients with excessive acid reflux , usually respond to PPI therapy. • Second are the patients with normal acid reflux parameters but a good correlation between their symptoms and acid reflux episodes. This group represents 30% to 50% of nonerosive GERD patients and, based on recent Rome IV criteria, is classified as “reflux hypersensitivity.” • The third group is characterized by normal acid exposure times and poor symptom correlation. This group is classified as “functional heartburn.
  45. 45. TREATMENT OF GERD • MEDICAL – includes both lifestyle modifications and pharmacologic interventions. • SURGICAL
  46. 46. LIFESTYLE CHANGES • Foods – • Acidic liquid such as cola, tea, citrus products such as orange, grapefruit, and tomato juice are direct esophageal irritants and will exacerbate symptoms in the GERD patient. • Coffee and chocolate can decrease LES pressure and may exacerbate reflux. • A high-fat meal will increase reflux frequency in both normals and patients with GERD. Fat may increase the risk of reflux by delaying gastric emptying. • Eating slowly will reduce reflux as will meals with smaller volume.
  47. 47. erosive esophagitis • male, older, and overweight and are more likely to have hiatal hernias • The clinical course of these patients is more predictable and associated with complications of GERD. • High relapse after discontinuation of PPI
  48. 48. • Body weight: • A BMI greater than 30 is associated with almost three times higher risk of frequent reflux symptoms. • Weight gain has been associated with an increased risk of symptoms of GERD and weight loss associated with a decrease in risk.
  49. 49. • Sleep and body position • Patients with nighttime GERD should begin the sleeping period with the left side down. - Decrease in transient lower esophageal sphincter relaxations (TLESRs) on the left side as compared to the right. • Refrain from eating within 2 to 3 hours of going to sleep - As reflux is more frequent in the first half of the sleep  Alcohol • Alcohol is a smooth muscle relaxant and reduces lower esophageal sphincter pressure (LESP). Should be used judiciously.
  50. 50. • Smoking • May increase esophageal sensitivity to acid by impairing intracellular regulation of pH. • Smoking cessation in individuals with GERD has been shown to reduce the number of upright reflux episodes.
  51. 51. Pharmacotherapy • Antisecretory therapy is still the choice for medical therapy for GERD. • Antacids are widely used as first-line treatment for the heartburn symptoms of GERD • Sucralfate • mucosal protective agent • Little or no place in normal modern therapy of GERD
  52. 52. H2 RECEPTOR ANTAGONISTS • antisecretory capabilities are best at night, with duration of acid inhibition longer when the drug is taken in the evening or before bedtime. • patients, particularly those with infrequent or mild symptoms can be managed long-term on as- needed or daily H2RAs. • Esophagitis healing rates with H2RAs rarely exceeded 60% after up to 12 weeks. • grades I and II esophagitis heal in 60% to 90% of patients, • grades III and IV heal in only 30% to 50% despite high-dose
  53. 53. Proton Pump Inhibitor • Superior efficacy compared with H2ras on the basis of their ability to maintain an intragastric Ph > 4 from 10 to 14 hours daily compared with Approximately 6 to 8 hours daily with the h2ras • Some patients need an increase in PPI dose because of incomplete symptom relief, extraesophageal symptoms, or Barrett esophagus. • Healing of even severe ulcerative esophagitis after 8 weeks in more than 80% of patients taking PPIs, compared with 51% on H2RAs and 28% receiving placebo.
  54. 54. • Recent approaches to enhance acid suppression with PPIs include immediate-release omeprazole and dexlansoprazole • Dexlansoprazole MR is the R-enantiomer of lansoprazole, with 2 distinct drug release periods (90 minutes and 4 to 5 hours after ingestion) • In a recent placebo-controlled study among 178 patients receiving twice-daily PPIs, stepping down to once-daily dexlansoprazole 30 mg, maintained excellent symptom relief over 6 weeks in 88% of patients.
  55. 55. Alginates • Alginic acid derivatives, or alginates, treat GERD via a unique mechanism by creating a mechanical barrier that displaces the postprandial acid pocket. • In the presence of gastric acid, they precipitate into a gel and form a raft that localizes to the acid pocket in the proximal stomach.
  56. 56. • showing fluorescein-labeled alginate on the luminal surface of the biopsy mucosa after 1 hour of washing in a neutral solution •Inhibition of pepsin and bile acids. Alginate can remove both pepsin and bile acids from gastric refluxate. •Alginates play a major role in the topical protection of the vulnerable and sensitive esophageal mucosa, reducing the risk of inflammation from gastric refluxate,
  57. 57. Prokinetics • Although prokinetics may theoretically alleviate the pathophysiology of GERD by increasing gastric and esophageal emptying, the evidence behind their clinical efficacy as add- on therapy over PPI is lacking. • Combination therapy did not have better efficacy than PPI alone for symptom control or endoscopic response, and the combination therapy was associated with worse adverse effects. • subset of patients with GERD who have delayed gastric emptying may benefit from the addition of prokinetics
  58. 58. Transient Lower Esophageal Sphincter Relaxation Inhibitors • only medication available that decreases • tLESRs is baclofen, a GABAB agonist used for many years to treat spasticity. • Baclofen (5 to 20 mg 3 times daily) significantly reduces tLESRs, decreases both acid and duodenal reflux, and improves symptoms in GERD patients treated for 4 weeks to several months.
  59. 59. ANTI REFLUX SURGERY Primary Indications for Antireflux Surgery (1) healthy patients with typical or atypical GERD symptoms well controlled on PPIs, desiring alternative therapy because of drug expense, poor medication compliance, or fear of possible long-term side effects; (2) patients with volume regurgitation and aspiration symptoms not controlled on PPIs (3) GERD complications such as peptic stricture, Barrett esophagus, or vocal cord injury
  60. 60. • Antireflux surgery reduces acid and nonacid GER by – increasing basal LES pressure, – decreasing tLESRs, – inhibiting complete LES relaxation
  61. 61. Choice of surgery Factors influencing : - • degree of esophageal shortening • disturbances of esophageal motility • prior operations and • local expertise with laparoscopic techniques
  62. 62. • Early uncomplicated disease : – Trans-abdominal Nissen (laparoscopic) fundoplication. superior operation with better long-term durability, but it causes more postoperative dysphagia and gas bloat symptoms. • Decreased motility : – Although surgery cannot directly influence esophageal motility in patients with GERD, Nissen fundoplication can lead to improvement in esophageal contraction amplitude.
  63. 63. • Normal length but decreased motility : – Complete fundoplication is discouraged. Toupet or Hill could be performed • Shortened esophagus : – Collis (esophageal lengthening) gastroplasty combined with an intra-abdominal or intrathoracic fundoplication
  64. 64. Post operative • Gas bloat syndrome • Dysphagia • 5-10% failure
  65. 65. Novel Endoscopic/Surgical Therapies • The newest approach is the transoral incisionless fundoplication which recreates at 200- to 270-degree value using polypropylene fasteners placed endoscopically. • over time the fasteners tend to dislodge, with a systematic review reporting GERD symptom recurrence in 60% of patients with a similar rate back on PPIs.
  66. 66. • Magnetic sphincter, which is a necklace of titanium beads with magnetic cores placed around the cardia, with minimal dissection of the hiatus.
  67. 67. • Use of electrical stimulation to the LES to improve LES pressure without interfering with LES relaxation
  68. 68. Complications of GERD • The most common fatal causes are hemorrhagic esophagitis, aspiration pneumonia, ulcer perforation, and rupture with severe esophagitis. • Peptic Esophageal Strictures – 7% to 23% of patients with untreated reflux esophagitis. – Peptic strictures are smooth-walled, tapered, circumferential narrowings in the lower esophagus, usually less than 1 cm long but occasionally extend to 8 cm – Dysphagia to solids , mild weight loss • Barrett’s Esophagus
  69. 69. • Thank You