Gastroesophageal Reflux Disease Arthur Harris M D GI

Gastroesophageal Reflux Disease Arthur Harris, M. D. GI Division, Jacobi Medical Center/NCBH Assistant Professor of Medicine, AECOM

Objectives n n n n Definition of GERD Epidemiology of GERD Pathophysiology of GERD Clinical Manifestations Diagnostic Evaluation Treatment Complications

Definition n 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

Physiologic vs Pathologic n Physiologic GERD • • • Post-prandial Short-lived Often asymptomatic TLSER’s No nocturnal sx n Pathologic GERD • • • Symptoms Mucosal injury Nocturnal sx

Epidemiology n n n About 44% of the US adult population have heartburn at least once a month 14% of Americans have symptoms weekly 7% have symptoms daily

Pathophysiology n n n 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

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

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

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

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

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

Trial of Medications n H 2 RA or PPI • Expect response in 2 -4 weeks • If no response Change from H 2 RA to PPI n Maximize dose of PPI n

Trial of Medications n If PPI response inadequate despite maximal dosage • Confirm diagnosis EGD n 24 hour p. H monitoring n

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

Ambulatory p. H Testing n 24 -hour p. H monitoring • Accepted standard for establishing or excluding presence of GERD for those patients who do not have mucosal changes • Trans-nasal catheter or a wireless, capsule shaped device

Ambulatory 24 hour p. H Monitoring -1 n n Physiologic study Quantify reflux in proximal/distal esophagus • % time p. H < 4 • De. Meester score n Symptom correlation

Ambulatory 24 hour p. H Monitoring -2 Normal GERD

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

Esophageal Manometry Limited role in GERD n Assess LES pressure, location and relaxation • Assist placement of 24 hour p. H catheter n Assess peristalsis • Prior to anti-reflux surgery

Patient with heartburn Initiate Rx with H 2 RA or PPI H 2 RA taken BID PPI taken QD No Good response Yes No Yes Frequent relapses No On demand Rx Increase to max dose QD or BID Maintenance therapy with lowest effective dose Yes Symptoms persist Good response No Consider EGD if risk factors present (> 45, white, male and > 5 yrs of sx) Confirm diagnosis EGD, ph monitor

GERD vs Dyspepsia n Distinguish from Dyspepsia • Ulcer-like symptoms-burning, epigastric pain • Dysmotility like symptoms-nausea, bloating, early satiety, anorexia n n Distinct clinical entity In addition to anti-secretory meds and an EGD, need to consider testing for Helicobacter pylori

Treatment n Goals of therapy • Symptomatic relief • Heal esophagitis • Avoid complications

Better Living n Lifestyle modifications • Avoid large meals • Avoid acidic foods (citrus/tomato), alcohol, caffeine, 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, NSAID’s) • Avoid clothing that is tight around the waist • Lose weight • Stop smoking

Treatment n Antacids • O-T-C acid suppressants and antacids may be 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

Treatment n Histamine H 2 -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

Treatment AGENT Cimetadine Tagamet EQUIVALENT DOSAGES 400 mg twice daily DOSAGE 400 -800 mg twice daily Famotidine Pepcid 20 mg twice daily 20 -40 mg twice daily Nizatidine Axid 150 mg twice daily Ranitidine Zantac 150 mg twice daily

Treatment n Proton Pump Inhibitors • Better control of symptoms with PPI’s vs H 2 RAs and better remission rates • Faster healing of erosive esophagitis with PPIs vs H 2 RAs

Treatment AGENT Esomeprazole Nexium EQUIVALENT DOSAGES 40 mg daily DOSAGE 20 -40 mg daily Omeprazole Prilosec 20 mg daily Lansoprazole Prevacid 30 mg daily 15 -30 mg daily Pantoprazole Protonix 40 mg daily Rabeprazole Aciphex 20 mg daily

Treatment n H 2 RAs vs PPI’s • 12 week freedom from symptoms n 48% vs 77% • 12 week esophagitis healing rate n 52% vs 84% • Speed of healing n 6%/wk vs 12%/wk

Treatment Modifications for Persistent Symptoms n Improve compliance n Optimize pharmacokinetics • Adjust timing of medication to 15 – 30 minutes before meals (as opposed to bedtime) • Allows for high blood level to interact with parietal cell proton pump activated by the meal n Consider switching to a different PPI

Treatment n Anti-reflux surgery - Indications • Failed medical management • Patient preference • GERD complications • Medical complications attributable to a large hiatal hernia • Atypical symptoms with pathologic reflux documented on 24 -hour p. H monitoring

Treatment n Anti-reflux surgery candidates • EGD proven esophagitis • ? Normal esophageal motility • Incomplete response to acid suppression

Treatment n Anti-reflux surgery (laparoscopic) • Tenets of surgery Reduce hiatal hernia n Repair diaphragm n Strengthen GE junction n Strengthen anti-reflux barrier via gastric wrap n 75 -90% effective at alleviating symptoms of heartburn and regurgitation n

Treatment n Post-surgery • 10% have solid food dysphagia • 2 -3% have permanent symptoms • 7 -10% have gas, bloating, diarrhea, nausea, early satiety • Within 3 -5 years, up to 52% of patients back on anti-reflux medications

Treatment n Endoscopic treatment • • • n Relatively new No clearly established indications 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 non-resorbable polymer into LES region

Complications n n n Erosive esophagitis Stricture Barrett’s esophagus

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

Complications n Esophageal stricture • Occurs as a result of healing of erosive esophagitis • May need dilation

Peptic Stricture Barium swallow Endoscopy

Complications n Barrett’s Esophagus • Columnar metaplasia of the esophagus • Associated with the development of adenocarcinoma

Complications n Barrett’s Esophagus • Acid damages lining of esophagus and causes chronic esophagitis • Damaged area heals in a metaplastic process with abnormal columnar cells replacing squamous cells • This specialized intestinal metaplasia can progress to dysplasia and adenocarcinoma

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

Complications n Barrett’s Esophagus • Manage in same manner as GERD • EGD every 3 years in patient’s without dysplasia • In patients with dysplasia, annual to even shorter interval surveillance is recommended

Summary n n n n Definition of GERD Epidemiology of GERD Pathophysiology of GERD Clinical Manifestations Diagnostic Evaluation Treatment Complications

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