Gastroesophageal Reflux Disease (GERD)

Overview

GERD is a family of conditions caused by the reflux of gastric contents into the esophagus, resulting in either troublesome symptoms or esophageal/extraesophageal manifestations. It affects 10–15% of adults in the United States. The spectrum of esophageal injury ranges from esophagitis to adenocarcinoma, with esophageal adenocarcinoma incidence rising two- to sixfold over the past 20 years (~9,200 cases/year in the U.S.) (Harrison's, p. 8868).

Anatomy & Pathophysiology

The key anatomical barrier against reflux is the lower esophageal sphincter (LES), supported by the crural diaphragm. GERD occurs when this barrier fails via:

Mechanism	Description
Transient LES Relaxations (TLESRs)	The most common cause; LES relaxes independent of swallowing, allowing reflux
Hypotensive LES	Persistently low resting LES pressure (<10 mmHg)
Hiatal Hernia	Displaces the LES above the diaphragm, disrupting the anti-reflux barrier
Impaired Esophageal Clearance	Reduced peristalsis prolongs acid exposure time
Delayed Gastric Emptying	Increases intragastric pressure and volume

Clinical Manifestations

Esophageal (Typical) Symptoms

Heartburn (pyrosis) — substernal burning, the hallmark symptom
Regurgitation — retrograde flow of gastric contents to mouth/pharynx
Dysphagia — suggests stricture or motility disorder
Odynophagia — pain on swallowing, suggests esophagitis

Extraesophageal (Atypical) Symptoms

Chronic cough, hoarseness, laryngitis
Non-cardiac chest pain
Asthma exacerbations
Dental erosions
Globus sensation

Complications (Spectrum of Injury)

The GI complications progress along a well-defined spectrum:

Erosive Esophagitis (EE) — mucosal breaks; graded by Los Angeles (LA) Classification (A–D)
Peptic Stricture — fibrotic narrowing from chronic acid injury
Barrett's Esophagus (BE) — intestinal metaplasia of the esophageal mucosa; precancerous
Esophageal Adenocarcinoma — the most feared complication; highest-risk progression from BE with dysplasia

GERD complications: peptic stricture, hiatal hernia, and Barrett's esophagus on imaging

Composite image showing (A) barium swallow with peptic stricture, (B) hiatal hernia on contrast radiography, and (C) Barrett's esophagus on endoscopy (salmon-colored mucosa).

Diagnosis

1. Clinical Diagnosis

Typical heartburn + regurgitation → empiric PPI trial is sufficient in uncomplicated cases.

2. Upper Endoscopy (EGD) — Indications

Alarm symptoms: dysphagia, weight loss, bleeding, anemia
Failure to respond to PPI therapy
Long-standing GERD (>5 years) to screen for Barrett's esophagus
Age >60 with new-onset symptoms

3. Ambulatory pH Monitoring (Gold Standard)

24-hour pH-impedance testing — measures acid and non-acid reflux events
Performed off PPI (for diagnosis) or on PPI (for treatment failure assessment)
Key metric: DeMeester score and percentage time pH <4

4. High-Resolution Manometry (HRM)

Not diagnostic for GERD but evaluates LES pressure and esophageal motility
Required before anti-reflux surgery

5. Barium Swallow

Detects hiatal hernia, strictures, and severe reflux
Low sensitivity; not recommended as primary diagnostic tool

Management

Step 1: Lifestyle Modifications

Intervention	Rationale
Elevate head of bed 6–8 inches	Reduces nocturnal reflux
Avoid lying down within 3 hrs of eating	Reduces postprandial reflux
Weight loss	Decreases intraabdominal pressure
Avoid triggers (fatty foods, caffeine, alcohol, chocolate, mint)	Reduces LES relaxation
Smoking cessation	Improves LES tone

Step 2: Pharmacological Therapy

Drug Class	Examples	Notes
PPIs (first-line)	Omeprazole, Pantoprazole, Esomeprazole	Taken 30–60 min before meals; most effective acid suppression
H2 Receptor Antagonists	Famotidine, Ranitidine	Second-line or add-on for nocturnal breakthrough
Antacids/Alginates	Tums, Gaviscon	Rapid but short-lived symptom relief
Prokinetics	Metoclopramide	Rarely used; side-effect profile limits use

On-demand PPI for mild/intermittent GERD
Daily PPI for erosive esophagitis, Barrett's esophagus, or frequent symptoms
Long-term PPI use: monitor for Mg²⁺/B12 deficiency, bone density, and C. difficile risk

Step 3: Surgical / Procedural Therapy (Refractory GERD)

Laparoscopic Nissen Fundoplication — gold standard surgical option; wraps gastric fundus 360° around LES
Partial fundoplication (Toupet/Dor) — preferred when esophageal motility is impaired
LINX device — magnetic sphincter augmentation; less invasive
Transoral Incisionless Fundoplication (TIF) — endoscopic option for select patients

Barrett's Esophagus Surveillance

Finding	Surveillance Interval
No dysplasia	Every 3–5 years
Low-grade dysplasia	Every 6–12 months or endoscopic eradication therapy
High-grade dysplasia	Endoscopic eradication therapy (RFA, EMR)

Key Differentials

Peptic ulcer disease (PUD)
Achalasia / esophageal motility disorder
Eosinophilic esophagitis (EoE)
Non-cardiac chest pain / angina
Functional dyspepsia
Gastroparesis

Source: Harrison's Principles of Internal Medicine, 21st Edition, p. 8868

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