Gastroesophageal Reflux Disease GERD

Pathophysiology

• Excessive transient relaxations of lower esophageal sphincter (LES) or incompetent LES

• Esophageal mucosal damage (esophagitis) due to prolonged contact with acid. etc.

• Hiatal hernia: contributes to J LES tone; acts as reservoir for refluxed gastric contents

Clinical manifestations

• Heartburn, atypical chest pain; regurgitation of stomach contents, water brash, dysphagia

• Cough (chronic nocturnal aspiration), asthma, hoarseness (vocal cord inflammation)

• Précipitants: large meals, supine position, fatty foods, caffeine, alcohol, cigarettes. CCB

Diagnosis

• Often based on Hx, trial of PP1 (although Se & Sp of improved sx after empiric PP1 for dx of

GERD are surprisingly low. 78% & 54% respectively) (Anrv* 2004; 140518)

• EGD to detect esophagitis. ulcer, Barretts esophagus, or stricture (jama 2002:287:1972)

• 24-h ambulatory esophageal pH monitoring if diagnosis is uncertain Treatment

• Lifestyle measures: avoid précipitants, small meals, avoid late meals, elevate head of bed

• Medical: antacids. Hî-blockers, PPI. prokinetic agents

• Surgical: fundoplication (often laparoscopic), success rate -90% (nejm 1992:326.786) Complications

• Esophagitis. Barrett's csopltogus (specialized intestinal metaplasia with 30-60 ■ Trisk of adenocarcinoma. 0.8% per y. nejm 1999:340825 & 2002:346:846). stricture

• If Barrett s found, endoscopic surveillance (eg. q 3 y) for dysplasia is warranted

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