GERD is a common condition where stomach acid refluxes into the esophagus, potentially causing symptoms like heartburn and damage to the esophagus. About 44% of adults experience heartburn monthly, with risk factors including obesity, smoking, and hiatal hernia. Diagnosis involves assessing symptoms, and testing may include pH monitoring or endoscopy. Treatment focuses on lifestyle changes and medications like PPIs to reduce acid production, while complications can include esophagitis, strictures, and Barrett's esophagus, a precursor to esophageal cancer. Surgery is an option for severe cases that do not respond to medical management.

1. Gastro esophageal Reflux Disease My room My mess ENT Central emergency

2. Gasroesophageal reflux disease (GERD)

4. Objectives Definition of GERD Epidemiology of GERD Pathophysiology of GERD Clinical Manisfestations Diagnostic Evaluation Treatment Complications

5. Definition American College of Gastroenterology (ACG) Symptoms OR mucosal damage produced by the abnormal reflux of gastric contents into the esophagus Often chronic and relapsing May see complications of GERD in patients who lack typical symptoms

6. Physiologic vs Pathologic Physiologic GERD Postprandial Short lived Asymptomatic No nocturnal sx Pathologic GERD Symptoms Mucosal injury Nocturnal sx

7. Epidemiology About 44% of the adult population have heartburn at least once a month 14% of adults have symptoms weekly 7% have symptoms daily These are US data In INDIA the prevalence is somewhat lesser but on an INCREASING trend

10. Pathophysiology Primary barrier to gastroesophageal reflux is the lower esophageal sphincter LES normally works in conjunction with the diaphragm If barrier disrupted, acid goes from stomach to esophagus

11. Clinical Manisfestations Most common symptoms Heartburn—retrosternal burning discomfort Regurgitation—effortless return of gastric contents into the pharynx without nausea, retching, or abdominal contractions

13. Clinical Manisfestations Dysphagia—difficulty swallowing Other symptoms include: Chest pain, water brash, globus sensation, odynophagia, nausea Extraesophageal manifestations Asthma, laryngitis, chronic cough

14. Extraesophageal Manifestations of GERD Pulmonary Asthma Aspiration pneumonia Chronic bronchitis Pulmonary fibrosis Other Chest pain Dental erosion ENT Hoarseness Laryngitis Pharyngitis Chronic cough Globus sensation Dysphonia Sinusitis Subglottic stenosis Laryngeal cancer

15. Potential Oral and Laryngopharyngeal Signs Associated with GERD Edema and hyperemia of larynx Vocal cord erythema, polyps, granulomas, ulcers Hyperemia and lymphoid hyperplasia of posterior pharynx Interarytenyoid changes Dental erosion Subglottic stenosis Laryngeal cancer

16. Pathophysiology of Extraesophageal GERD

18. Diagnostic Evaluation If classic symptoms of heartburn and regurgitation exist in the absence of “alarm symptoms” the diagnosis of GERD can be made clinically and treatment can be initiated

19. Alarms Alarm Signs/Symptoms Dysphagia Early satiety GI bleeding Odynophagia Vomiting Weight loss Iron deficiency anemia

20. When to Perform Diagnostic Tests Uncertain diagnosis Atypical symptoms Symptoms associated with complications Inadequate response to therapy Recurrent symptoms Prior to anti-reflux surgery

21. Diagnostic Tests for GERD Trial of H2RA/PPI Barium swallow Ambulatory pH monitoring Esophagogastroduodenoscopy(EGD) Esophageal manometry

22. Trial of Medications H2RA or PPI Expect response in 2-4 weeks If no response Change from H2RA to PPI Maximize dose of PPI

23. Trial of Medications If PPI response inadequate despite maximal dosage Confirm diagnosis EGD 24 hour pH monitor

24. Barium Swallow Useful first diagnostic test for patients with dysphagia Stricture (location, length) Mass (location, length) Bird’s beak Hiatal hernia (size, type) Limitations Detailed mucosal exam for erosive esophagitis, Barrett’s esophagus

25. Ambulatory 24 hr. pH Monitoring Physiologic study Quantify reflux in proximal/distal esophagus % time pH < 4 DeMeester score Symptom correlation

26. Ambulatory 24 hr. pH Monitoring Normal GERD

27. Wireless, Catheter-Free Esophageal pH Monitoring Improved patient comfort and acceptance Continued normal work, activities and diet study Longer reporting periods possible (48 hours) Maintain constant probe position relative to SCJ Potential Advantages

28. Esophagogastrodudenoscopy Endoscopy (with biopsy if needed) In patients with alarm signs/symptoms Those who fail a medication trial Those who require long-term tx Lacks sensitivity for identifying pathologic reflux Absence of endoscopic features does not exclude a GERD diagnosis Allows for detection, stratification, and management of esophageal manisfestations or complications of GERD

29. Esophageal Manometry investigation of choice in diffuse esophageal spasm(AI08) Assess LES pressure, location and relaxation Assist placement of 24 hr. pH catheter Assess peristalsis Prior to antireflux surgery Limited role in GERD

30. Patient with heartburn Iniate tx with H2RA or PPI H2RA taken BID Good response Frequent relapses On demand tx PPI taken QD Good response Maintenance therapy with lowest effective dose Symptoms persist Consider EGD if risk factors present ( > 45, white, male and > 5 yrs of sx) Increase to max dose QD or BID Good response Confirm diagnosis EGD, ph monitor No Yes Yes No Yes Yes No No

31. Differential diagnosis Angina pectoris Gastritis Peptic ulcer disease Gallstones pancreatitis Achalasia cardia Carcinoma oesophagus

32. Treatment Goals of therapy Symptomatic relief Heal esophagitis Avoid complications

33. Better Living Lifestyle modifications Avoid large meals Avoid acidic foods (citrus/tomato), alcohol, caffiene, chocolate, onions, garlic, peppermint Decrease fat intake Avoid lying down within 3-4 hours after a meal Elevate head of bed 4-8 inches Avoid meds that may potentiate GERD (CCB, alpha agonists, theophylline, nitrates, sedatives, NSAIDS) Avoid clothing that is tight around the waist Lose weight Stop smoking

34. 1. Orr WC, et al. Gastroenterology . 1984;86:814-819. 2. Orr WC, et al. Am J Gastroenterol . 2000;95:37-42. 3. Orr WC, et al. Am J Gastroenterol . 1994;89:509-512. 4. Kjellén G, Tibbling L. Scand J Gastroenterol . 1978;13:283-288. Sleep May Impair Esophageal Acid Clearance  Gravity-Mediated Drainage 4  Esophageal Acid Clearance 1–3  Salivary Flow and Swallowing 1 Asleep Awake Factors FACTORS THAT MAY CONTRIBUTE TO INCREASED ESOPHAGEAL ACID EXPOSURE DURING SLEEP

35. Treatment Antacids Over the counter acid suppressants and antacids appropriate initial therapy Approx 1/3 of patients with heartburn-related symptoms use at least twice weekly More effective than placebo in relieving GERD symptoms

36. Treatment Histamine H2-Receptor Antagonists More effective than placebo and antacids for relieving heartburn in patients with GERD Faster healing of erosive esophagitis when compared with placebo Can use regularly or on-demand

37. Treatment AGENT EQUIVALENT DOSAGE DOSAGES Cimetadine 400mg twice daily 400-800mg twice daily Famotidine 20mg twice daily 20-40mg twice daily Nizatidine 150mg twice daily 150mg twice daily Ranitidine 150mg twice daily 150mg twice daily

38. Treatment Proton Pump Inhibitors Better control of symptoms with PPIs vs H2RAs and better remission rates Faster healing of erosive esophagitis with PPIs vs H2RAs

39. Treatment AGENT EQUIVALENT DOSAGE DOSAGES Esomeprazole 40mg daily 20-40mg daily Omeprazole 20mg daily 20mg daily Lansoprazole 30mg daily 15-10md daily Pantoprazole 40mg daily 40mg daily Rabeprazole 20mg daily 20mg daily

40. Treatment H2RAs vs PPIs 12 week freedom from symptoms 48% vs 77% 12 week healing rate 52% vs 84% Speed of healing 6%/wk vs 12%/wk

41. NOT ALL PROTON PUMPS ARE ACTIVE AT ANY GIVEN TIME 1. Del Valle J, et al. Acid peptic disorders. In: Yamada et al, eds. Textbook of Gastroenterology . 4th ed. Philadelphia, Pa: Lippincott Williams and Wilkins; 2003:1321-1376. Unstimulated proton pumps Active proton pumps Unstimulated proton pumps in cytoplasmic tubules 1. Blair JA, et al. J Clin Invest. 1987;79:582-587. 2. Sachs G. Pharmacotherapy . 1997;17:22-37. H 2 = Histamine ACh = Acetylcholine Proton pumps become activated in response to food 1 Inactive Parietal Cell After activation, the parietal cell undergoes a series of changes, allowing proton pumps to reach the surface of the parietal cell 1 Active Parietal Cell Only active proton pumps can secrete acid 1 However, not all pumps become activated 1,2 ATPase ATPase MOA Gastrin H 2 ACh H+ H+ H+ H+ K+ K+ K+ K+

42. PPIs ONLY BIND TO ACTIVE PROTON PUMPS Acid is required to convert a PPI into its active form 1 1. Del Valle J, et al. Acid peptic disorders. In: Yamada et al, eds. Textbook of Gastroenterology . 4th ed. Philadelphia, Pa: Lippincott Williams and Wilkins; 2003:1321-1376. PPIs only bind to active proton pumps 1 Unstimulated proton pumps remain MOA PPI PPI PPI PPI

43. PPI USE AND INFECTION RISK: IS THERE A RELATIONSHIP? Gastric acid plays a role in eliminating ingested bacteria from the digestive tract 1 PPI use associated with Enteric infection such as Clostridium difficile Nonenteric infection such as community-acquired pneumonia C. difficile Safety

44. Treatment Antireflux surgery Failed medical management Patient preference GERD complications Medical complications attributable to a large hiatal hernia Atypical symptoms with reflux documented on 24-hour pH monitoring

45. Treatment Antireflux surgery candidates EGD proven esophagitis Normal esophageal motility Partial response to acid suppression

46. Treatment Antireflux surgery Tenets of surgery Reduce hiatal hernia Repair diaphragm Strengthen GE junction Strengthen antireflux barrier via gastric wrap 75-90% effective at alleviating symptoms of heartburn and regurgitation

48. (Nissen’s)

49. Complete vs. partial fundoplication Complete – Nissen fundoplication Ant. partial fundoplication  Thal/Dor procedure Post. partial fundoplication  Toupet procedure

50. Laparoscopic Nissen Fundoplication

51. Treatment Postsurgery 10% have solid food dysphagia 2-3% have permanent symptoms 7-10% have gas, bloating, diarrhea, nausea, early satiety Within 3-5 years 52% of patients back on antireflux medications

52. Treatment Endoscopic treatment Relatively new No definite indications Select well-informed patients with well-documented GERD responsive to PPI therapy may benefit Three categories Radiofrequency application to increase LES reflux barrier Endoscopic sewing devices Injection of a nonresorbable polymer into LES area

53. Complications Erosive esophagitis Stricture Barrett’s esophagus

54. Complications Erosive esophagitis Responsible for 40-60% of GERD symptoms Severity of symptoms often fail to match severity of erosive esophagitis

55. Complications Esophageal stricture Result of healing of erosive esophagitis May need dilation

56. Peptic Stricture Barium Swallow Endoscopy

57. Esophageal Stricture: Dilating Devices

58. TTS Balloon Dilation of a Peptic Stricture

59. Complications Barrett’s Esophagus Columnar metaplasia of the esophagus (AIIMS06) Associated with the development of adenocarcinoma (AIMS97,06)

60. Barrett’s Esophagus

61. Complications Barrett’s Esophagus Acid damages lining of esophagus and causes chronic esophagitis (AIIMS98) Damaged area heals in a metaplastic process and abnormal columnar cells replace squamous cells This specialized intestinal metaplasia can progress to dysplasia and adenocarcinoma

62. Complications Barrett’s Esophagus Manage in same manner as GERD EGD every 3 years in patient’s without dysplasia In patients with dysplasia annual to shorter interval surveillance

63. Complications Patient’s who need EGD Alarm symptoms Poor therapeutic response Long symptom duration “Once in a lifetime” EGD for patient’s with chronic GERD becoming accepted practice Many patients with Barrett’s are asymptomatic

64. Esophageal Cancer Barium Swallow Endoscopy

65. MCQ’s Most prevalent esophageal cancer worldwide (AI91) Most common site of Ca oesophagus (AIIMS 97) Most common site for squamous cell Ca (AI 01) Most common site of esophageal adenocarcinoma (AIIMS 96,2000)

66. MCQ’s Most common site for Ca oesophagus in india Predisposing fators for Ca oesophagus are all except a-plummer vinson syn b-tulosis palmaris c-gerd d benzene therapy

67. MCQ’s Chemotherapy regimens for Ca oesophagus have improved with the use of (AI96) Commonest adverse effect of cisplatin (AIIMS01) Best substitute for esophagus after esophagectomy (AI96)

68. Summary Definition of GERD Epidemiology of GERD Pathophysiology of GERD Clinical Manisfestations Diagnostic Evaluation Treatment Complications

69. ?QUESTIONS?

70. A slideshow presentation Prepared by Dr. ZEESHAN AHMAD under guidance of DR(Prof)CHANDRA SHEKHAR Head ENT deptt & DR MK VERMA Assoc prof ENT deptt THANK YOU