Gastroesophageal reflux disease and antireflux surgery

1. Brannon Hyde, MD Gastroesophageal reflux disease and antireflux surgery

2. Learning objectives • Understand the natural history of reflux disease • Understand how to identify candidates for antireflux surgery • Understand the complications of antireflux surgery and patient’s satisfaction with surgery

3. Why do we care about reflux? • Americansexperience reflux symptoms • 44% monthly • 20% weekly • 4-7% daily • Most common gastrointestinal diagnosis on outpatient physician visits • Frequency and severity does not predict esophagitis, stricture, or cancer development

4. Definition of GERD • Montreal consensus panel (44 experts): “a condition which develops when the reflux of stomach contents causes troublesome symptoms and/or complications” • Troublesome—patient gets to decide when reflux interferes with lifestyle Vakil N, et al. Am J Gastroenterol 2006;101:1900

5. Clinical presentation • Heartburn • 1-2 hours after eating, often at night, antacid relief • Regurgitation • Spontaneous return of gastric contents proximal to GE jxn; less well relieved with antacids • Dysphagia (40%)—difficulty with swallowing should prompt search for pathologic condition

6. Clinical presentation • Atypical symptoms (20-25%) • Cough • Asthma • Hoarseness • Non-cardiac chest pain

7. Diagnosis • Diagnosis based on symptoms alone is correct in only 2/3 patients • Differential (ALL CAN KILL YOU!) • Achalasia • Diffuse esophageal spasm • Other esophageal motility disorder • Cancer • Ulcer disease • Coronary artery disease

8. So I’ve got GERD, what’s going to happen to me? • Spectrum of disease theory: Nonerosive disease  erosive disease  Barrett’s  esophageal adenocarcinoma Am J Gastroenterol 2004;99:946.

9. 3,894 patients had baseline and repeat endoscopy at 2 years, regardless of symptoms. Conclusion: progression and regression occur despite PPI therapy ProGERD study Am J Gastroent 2006;101:2457-62 Severe esophagitis Mild esophagitis

10. So I can diagnose it, and I know how bad it can get, but why does heartburn and regurgitation happen in the first place? Answer: alteration from normal physiology Normally, the lower esophageal sphincter exists as a zone of high pressure between esophagus and stomach; when the HPZ is lost, reflux occurs

11. Proximal esophagus Swallow • Transducer tracing identifies the LES • High pressure drops only after a swallow or when fundus is distended with gas (to belch) Distal esophagus Distal esophagus Distal esophagus Distal esophagus Relaxation of LES Gastric baseline

12. Physiology of antireflux barrier • Three components of high pressure zone • Absolute pressure • Overall length • Intra-abdominal length

13. Overall length shortens as stomach distends, increasing the pressure necessary to maintain competence (neck on a balloon)

14. Physiology of antireflux barrier • If intra-abdominal length is short, LES pressure can be overcome by small increases in intra-abdominal pressure • Increased abdominal pressure needs even distribution over high pressure zone abdominal length to prevent reflux

15. Normal physiology If sufficient intraabdominal length is present, squeeze (increased abdominal pressure) will occur around “neck of balloon,” and reflux will not occur

16. Physiology of antireflux barrier

17. Pathophysiology of GERD • Fundic distention (overeating) & delayed gastric emptying (high fat) • Lower esophageal sphincter is pulled distally by expanding fundus • Squamous epithelium exposed to gastric juice • Repeated exposure  columnarization

18. What does my body do to compensate for reflux esophagitis? • Compensation: • Increased swallowing  saliva bathes injured mucosa, alleviating discomfort • Results in aerophagia, bloating, and belching • Distention leads to further repetitive injury to the terminal squamous epithelium in distal esophagus

19. Pathophysiology of GERD • Extension of inflammation into muscularis propria causes progressive loss in length and pressure of the LES—”esophageal shortening” • Loss of LES leads to regurgitation, heartburn, and subsequent severe esophagitis

20. What role does a hiatal hernia play? • Greater gastric dilatation is necessary to open LES in patients with intact angle of HIS compared to those with a hiatal hernia • Reflux occurs easier < 3 cm > 3 cm

21. So I have a defective sphincter, what complications will I have? • Esophagitis (mucosal injury) with or without heartburn • Reflux chest pain syndrome • Respiratory complications • Metaplastic and neoplastic complications

22. Why is esophagitis bad? • Acid alone does minimal damage, but is highly toxic in combination with pepsin • Bile reflux alone does minimal damage, but when coupled with gastric acid, is destructive to esophageal mucosa • Decrease acid (with PPI or surgery), and esophageal lining heals

23. What is reflux chest pain syndrome? • Heartburn without esophagitis • bile salts inhibit pepsin • acid pH inactivates trypsin • pain comes from acidic gastric juice breaking mucosal barrier and irritating nerve endings

24. Respiratory complications • Reflux and aspiration of gastric contents induces asthma • Correlation between hiatal hernia and pulmonary fibrosis • Pathologic acid exposure often seen in proximal esophagus in patients with asthma • Simultaneous tracheal and esophageal pH monitoring shows acidification of trachea in concert with esophagus

25. What metaplastic complications can arise? • Norman Barrett (1950) first described the process whereby the esophageal squamous epithelium changes to columnar epithelium • Occurs in 7-10% of patients with GERD • Factors predisposing to Barrett’s • Early-onset GERD • Abnormal LES or motility disorder • Mixed reflux of gastric and duodenal contents

26. What are the neoplastic complications? Goblet cells • Barrett’s metaplasia harbors dysplasia in 15-25% • 5-10% is high-grade dysplasia High grade dysplasia; structure of glands becoming disorganized

27. So I understand a little about reflux; who needs an operation? • Need for continuous drug treatment or escalating dose of PPI • Relatively young • Financial burden or noncompliance with PPI • Patient choice

28. How do you know I’m a candidate for surgery? • Establish GERD as underlying cause of symptoms • Estimate risk of progressive disease • Determine presence or absence of esophageal shortening • Evaluate esophageal body function

29. How do you know I’m a candidate for surgery? • Factors predictive of successful outcome following antireflux surgery (n = 199) • Abnormal score on 24-hour esophageal pH monitoring (p < 0.001) • Presence of typical symptoms of GERD (heartburn and regurgitation) (p< 0.001) • Symptomatic improvement in response to acid suppressive therapy (p = 0.02) J Gastrointest Surg 1999;3:292-300

30. What specific studies do I need preoperatively? • Endoscopy • 24-hour ambulatory pH monitoring • Radiograph • Esophageal body and gastric function

31. Preoperative evaluation: endoscopy • Amounts to the physical examination • Strictures or large hiatal hernia may indicate shortened esophagus • High-grade dysplasia or a mass in the esophageal, gastric, or duodenal lumen will change management

32. Preoperative evaluation: 24-hour pH monitoring • Rationale: gold standard for diagnosis of GERD • Quantifies actual time the esophageal mucosa is exposed to gastric juice • Measures the ability of the esophagus to clear refluxed acid

33. Preoperative evaluation: 24-hour pH monitoring • Correlates esophageal acid exposure with patients symptoms • Without abnormal pH study, surgery is unlikely to benefit • Gives a composite score (Johnson-DeMeester score) highly sensitive and specific (>96%) for diagnosing GERD

34. Johnson-DeMeester normal values for esophageal pH < 4 (n = 50) J Clin Gastroenterol 8(suppl. 1):52-58, 1986.

35. Preop evaluation: swallow study • Only 40% of patients with classic symptoms of GERD will have reflux observed on radiography • Assess for: • Esophageal shortening • Hiatal hernia (80%) • Paraesophageal hernia • Stricture or obstructing lesion • Beading or corkscrewing (motility disorders)

36. Manometry Rules out esophageal motility disorders Esophageal body dysfunction (achalasia or aperistalsis) should change management.

37. So I have reflux, and I think I want surgery; what surgery do I have? • The most common antireflux operation is the laparoscopic fundoplication • Crural dissection, identification and preservation of both vagi • 25% have left hepatic artery coming from left gastric artery in the gastrohepatic ligament • Circumferential dissection of esophagus

38. So I have reflux, and I want surgery; what surgery do I have? • Elements of laparoscopic Nissen • Crural closure • Fundic mobilization by division of short gastrics • Creation of short, loose fundoplication by enveloping anterior and posterior wall around lower esophagus

39. That operation looks nice, are people satisfied with it? • Patient satisfaction is high (86-97%) • Long-term symptom relief (heartburn and regurgitation) in 84-97% • Symptomatic failure rate 3-13% • heartburn and regurgitation • Does not correlate with acidic reflux exposure • OPERATION DID NOTHING for 3-13%! Surgeon, August 2009:224.

40. How will I feel after that operation? • Bloating and increased flatulence (9-53%) • Most common side effect • Different scoring systems account for range • Pre-operative symptom scores are largely unknown Surgeon, August 2009:224.

41. What are the real bad things that can happen to me? • Review of 10,489 laparoscopic antireflux procedures • Complications • Wrap herniation (early) 1.3% • Pneumothorax 1.0% • All others < 1% (perforation, hemorrhage, pneumonia, abscess, splenic injury, trocar hernia, effusion, PE, ulcer, atelectasis, wound infection, MI, splenectomy) JACS 2001: 193(4); 428-39

42. How will I feel several months later? • Early dysphagia • usually transient (<6 weeks) • Persistent side effects (>1 month) • Bloating 9% • Reflux 4% • Dysphagia 3% • Often poorly defined JACS 2001: 193(4); 428-39 Surgeon, August 2009:224.

43. How do patients fare a decade down the line? • 10-year follow-up of 250 patients • 83% highly satisfied with outcome • 84% had good or excellent control of heartburn • 17% revision operation (usually 3-7%) • Recurrent hiatal hernia, dysphagia, reflux, bleeding (early takeback protocol for dysphagia) • 21% used acid-suppressive medication JACS 2007;205:570

44. Well, do I have to take the purple pill after the operation? • Use of acid-suppressive medication after antireflux surgery varies (21-62%) • But, only 20-30% with “reflux-like” symptoms after surgery have positive pH studies JACS 2007;205:570

45. Series are great, Doc, but what about a randomized trial? • Randomized trial comparing treatment of GERD with omeprazole (n = 154) and antireflux surgery (n = 144) • Treatment success—no symptoms or esophagitis (p < 0.002): • 67% surgical • 47% medical • Dysphagia, bloating, rectal flatulence common in surgical group Brit J Surg 2007;94:198.

46. Does surgery offer any benefit to avoiding cancer? • Cancer risk in patient with reflux symptoms is < 1 in 10,000 per patient year • No benefit to avoidance of Barrett’s or adenocarcinoma with surgery compared to PPI therapy • Low morbidity and mortality risks associated with laparoscopic antireflux surgery dwarf potential benefit of avoiding cancer Gastroent 2008;135:1392.

47. What does all of this mean, should I have surgery or not? • Surgery wins over PPI’s if you don’t mind trading heartburn and reflux for bloating, inability to belch, and excessive flatulence Not in everybody, BUT IT COULD BE YOU! • Nevertheless, 86-97% of patients are satisfied with surgery Gastroent 2008;135:1392.

48. Doc, with all that bloating, do you have to make the wrap so tight? Toupet Nissen 270 degree wrap Anterior (Dor)

49. So you don’t have to make it so tight? Great! • Complete fundoplication offers superior protection to reflux • Increased incidence of dysphagia, inability to belch, and excessive flatus • Partial wraps offer less protection against reflux, but also less symptoms • Up to 51% may have pathologic esophageal acid exposure on 24-hour pH monitoring Surg Endos 1997;11:1080.

50. So partial wraps really don’t help to stop reflux; so who needs one? • Complete now considered superior to partial even in patients with weak esophageal peristalsis • Exceptions: • achalasia—anterior wrap utilized with myotomy • Aperistalis (ie, scleroderma)