GERD: Acid Reflux, Causes and Treatment

Gastroesophageal reflux disease (GERD) — known as acid reflux disease — occurs when stomach contents, including acid and bile, reflux abnormally and persistently into the oesophagus, causing troublesome symptoms and/or mucosal damage. It is one of the most prevalent gastrointestinal conditions worldwide, affecting approximately 20% of adults in Western countries and up to 10–15% in East Asia — with prevalence rising rapidly in China alongside westernisation of diet and lifestyle.

GERD has a significant impact on quality of life — chronic heartburn and regurgitation disrupt sleep, restrict diet, and impair work performance. Left unmanaged, GERD can cause oesophageal mucosal injury (oesophagitis), oesophageal stricture, and — in a subset of patients — Barrett's oesophagus, a pre-malignant condition that can progress to oesophageal adenocarcinoma.

How Reflux Occurs

Under normal conditions, the lower oesophageal sphincter (LOS) — a zone of tonically contracted smooth muscle at the junction of the oesophagus and stomach — acts as a one-way valve, preventing gastric contents from entering the oesophagus. Swallowing and belching cause transient LOS relaxations (TLOSRs) that allow a small degree of normal reflux.

In GERD, the LOS is dysfunctional — either through:

1. Reduced LOS basal tone — allowing persistent upward reflux, particularly in supine position and with increased intra-abdominal pressure; associated with obesity, pregnancy, and certain medications
2. Excessive transient LOS relaxations (TLOSRs) — the most common mechanism in non-obese GERD; episodes of inappropriate LOS relaxation allow acid to reflux even with normal basal tone
3. Hiatal hernia — displacement of the gastro-oesophageal junction through the diaphragmatic hiatus into the chest; disrupts the anti-reflux barrier and is present in the majority of patients with severe oesophagitis

The oesophageal mucosa lacks the protective mucus layer and acid-buffering capacity of the stomach — repeated acid exposure causes inflammation, erosion, and eventually structural damage.

Risk Factors

Risk Factor	Mechanism
Obesity / central adiposity	Increased intra-abdominal pressure; higher frequency of TLOSRs; adipose-derived hormones alter LOS function
Hiatal hernia	Disrupts anatomical anti-reflux barrier
Pregnancy	Progesterone reduces LOS tone; uterus increases intra-abdominal pressure
Smoking	Reduces LOS tone; impairs oesophageal acid clearance
Dietary triggers	Fatty foods, chocolate, peppermint, alcohol, coffee, citrus — transiently relax LOS or delay gastric emptying
Large meals / late eating	Distension relaxes LOS; recumbency after meals promotes reflux
Medications	Calcium channel blockers, nitrates, anticholinergics, tricyclics, bisphosphonates — reduce LOS tone or directly irritate mucosa
Connective tissue disorders	Scleroderma — LOS atony and impaired oesophageal peristalsis

Symptoms

Typical Symptoms

Heartburn (pyrosis) — the cardinal symptom; a burning discomfort or pain rising from the epigastrium into the retrosternal area (behind the breastbone), often reaching the throat; typically worst after meals, when bending forward, and lying down; relieved (transiently) by antacids or sitting upright.

Regurgitation — effortless return of gastric contents (acid or food) into the mouth or throat without the muscle effort of vomiting; often associated with a sour or bitter taste; may cause waterbrash (sudden mouth filling with saliva as a vagal response to acid in the oesophagus).

Atypical / Extraoesophageal Symptoms

GERD can manifest without classic heartburn:

• Chronic cough — acid reflux triggering vagal reflex cough; most prominent when supine or after meals; often misdiagnosed and undertreated
• Laryngopharyngeal reflux (LPR) — acid reaching the pharynx and larynx; causes throat clearing, hoarseness, globus sensation (lump in throat), and chronic throat irritation
• Asthma exacerbation — acid-triggered bronchospasm; GERD is a common trigger in difficult-to-control asthma
• Non-cardiac chest pain — oesophageal spasm from acid exposure; mimics cardiac angina; must be distinguished by cardiac evaluation before attributing to GERD
• Dental erosion — chronic acid exposure to teeth during sleep-related reflux
• Sleep disturbance — nocturnal reflux frequently disrupts sleep quality

Alarm Symptoms Requiring Urgent Investigation

• Dysphagia (difficulty swallowing) — suggests peptic stricture, oesophageal cancer, or achalasia
• Odynophagia (painful swallowing)
• Unintentional weight loss
• Haematemesis or melaena (GI bleeding)
• Anaemia
• Age >55 with new reflux symptoms (new-onset heartburn at this age requires endoscopy to exclude malignancy)

Diagnosis

Empirical PPI Trial

In typical GERD without alarm features, a 4-week empirical trial of once-daily proton pump inhibitor (PPI) is both diagnostic and therapeutic. Substantial symptom improvement strongly supports a GERD diagnosis. This approach is appropriate in patients <55 without alarm features.

Upper GI Endoscopy (Gastroscopy)

Endoscopy allows direct visualisation of the oesophageal mucosa and is used to:

• Diagnose and grade oesophagitis (Los Angeles Classification: grades A–D)
• Diagnose Barrett's oesophagus — metaplastic columnar mucosa replacing squamous oesophageal epithelium
• Exclude oesophageal cancer, peptic strictures, eosinophilic oesophagitis, and other causes of symptoms
• Obtain biopsies from Barrett's mucosa for dysplasia surveillance

Los Angeles Classification of Oesophagitis:

• Grade A: ≥1 mucosal break ≤5 mm, not extending between mucosal folds
• Grade B: ≥1 mucosal break >5 mm, not extending between mucosal folds
• Grade C: Mucosal breaks extending between folds but <75% of oesophageal circumference
• Grade D: Mucosal breaks ≥75% of oesophageal circumference

Endoscopy in GERD is normal (non-erosive reflux disease — NERD) in approximately 50–70% of patients, even with significant symptoms.

24-Hour pH Monitoring / pH-Impedance Study

The gold standard for objective acid exposure measurement. A pH probe (or combined pH-impedance catheter) placed in the distal oesophagus records acid and non-acid reflux events and correlates them with symptoms over 24 hours. Essential for:

• Confirming GERD diagnosis before anti-reflux surgery
• Evaluating patients with typical symptoms who fail PPI therapy
• Distinguishing true GERD from functional heartburn

Wireless Bravo pH capsule — a small capsule attached to the oesophageal wall via endoscopy; records pH for 48–96 hours without nasal catheter; well tolerated.

Oesophageal Manometry

High-resolution manometry maps oesophageal pressure along the entire length, characterising LOS tone, oesophageal peristalsis, and the presence of hiatal hernia. Essential before anti-reflux surgery to exclude achalasia and severe peristaltic dysfunction.

Treatment

Lifestyle Modifications

Effective for mild GERD and as adjuncts to medication:

• Weight loss — even modest weight loss reduces reflux frequency and severity; the most impactful lifestyle intervention
• Elevate head of bed (15–20 cm) or use a wedge pillow — reduces nocturnal reflux
• Avoid eating within 3 hours of bedtime
• Dietary triggers — identify and avoid personal triggers (fatty foods, alcohol, coffee, chocolate, citrus, peppermint)
• Smoking cessation
• Avoid tight clothing

Proton Pump Inhibitors (PPIs)

The cornerstone of GERD pharmacotherapy — the most effective acid suppression class available:

Examples: omeprazole, esomeprazole, lansoprazole, pantoprazole, rabeprazole

Dosing: taken 30–60 minutes before the largest meal. Once-daily dosing for standard GERD; twice-daily for severe oesophagitis, Barrett's oesophagus, or refractory symptoms.

PPIs heal oesophagitis in 80–90% of patients within 8 weeks. Symptom relief in 70–80% of those with NERD.

Long-term use: for erosive oesophagitis or Barrett's oesophagus, long-term PPI therapy is required to prevent relapse and reduce cancer risk. Concerns about long-term side effects (magnesium deficiency, bone density, kidney disease, C. difficile, small intestinal bacterial overgrowth) are real but modest in magnitude — benefits outweigh risks in appropriate patients.

Potassium-competitive acid blockers (P-CABs): vonoprazan (approved in Japan, South Korea, China) — faster onset and longer acid suppression than PPIs; particularly effective for severe oesophagitis and H. pylori eradication.

H2-Receptor Antagonists

Famotidine, ranitidine (withdrawn due to NDMA contamination) — weaker acid suppression than PPIs; useful for on-demand/intermittent relief; rapid onset for breakthrough heartburn.

Alginate-based and Antacid Preparations

Gaviscon (alginate + antacid) — forms a raft above the gastric contents, mechanically reducing reflux episodes; effective for post-prandial and positional heartburn.

Anti-Reflux Surgery

For patients who prefer to discontinue lifelong medication, have significant regurgitation not controlled by PPIs (PPIs reduce acid but not the volume of reflux), or have large hiatal hernias causing mechanical symptoms:

Laparoscopic Nissen fundoplication — the most common anti-reflux operation. The fundus of the stomach is wrapped 360° around the lower oesophagus, reinforcing the LOS and reducing TLOSRs. Performed laparoscopically as a 1–2 night inpatient procedure.

• Highly effective: 85–90% of appropriately selected patients achieve long-term relief from heartburn and regurgitation and discontinue PPIs
• Requires careful patient selection (objective GERD confirmation by pH study; normal oesophageal motility; ideally reducible hiatal hernia)
• Side effects: dysphagia (usually transient), bloating, inability to belch (gas-bloat), dysphagia to solids in a minority
• Partial fundoplication (Toupet 270°) — less dysphagia risk; used in patients with impaired peristalsis

Magnetic Sphincter Augmentation (LINX device) — a ring of magnetic beads placed around the LOS laparoscopically; allows swallowing by separating, then closes to prevent reflux. Reversible; good outcomes; growing adoption.

Endoscopic anti-reflux procedures: radiofrequency energy (Stretta), transoral incisionless fundoplication (TIF) — moderate evidence; may suit selected patients with small hiatal hernias.

Barrett's Oesophagus — Surveillance and Endoscopic Treatment

Barrett's oesophagus (columnar metaplasia of the oesophagus) is a precursor to oesophageal adenocarcinoma. Management:

• Ongoing PPI therapy — high-dose PPI reduces acid exposure and may reduce cancer risk
• Endoscopic surveillance — biopsies every 2–5 years (depending on segment length and dysplasia grade)
• Endoscopic eradication therapy (EET):
  • Radiofrequency ablation (RFA) — thermal ablation of Barrett's mucosa; standard treatment for dysplastic Barrett's; achieves eradication in 80–90% of cases
  • Endoscopic mucosal resection (EMR) or endoscopic submucosal dissection (ESD) — for visible nodules or raised lesions within Barrett's (early cancer or high-grade dysplasia)

GI and Reflux Care in China

China's gastroenterology centres offer:

• High-definition diagnostic gastroscopy: chromoendoscopy, NBI magnification, and systematic Barrett's biopsy protocols
• 24-hour pH-impedance monitoring and oesophageal manometry: wireless Bravo pH capsule available at leading centres
• Vonoprazan (P-CAB) prescribing: advanced acid suppression — available in China ahead of many Western countries
• Laparoscopic fundoplication: experienced upper GI surgeons for anti-reflux surgery; minimally invasive approach standard
• Barrett's ablation programme: RFA and ESD/EMR for dysplastic Barrett's oesophagus at specialist endoscopy centres
• Cost: care in China is generally less expensive than UK private treatment, but the hospital prices each case individually — ask us for the written quote before you commit.
• Full English care navigation from diagnostic assessment through treatment and follow-up

Contact a ChinaMedicalTour care navigator to arrange a reflux assessment, endoscopy, or anti-reflux surgery consultation.

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Medical content based on MSD Manuals and international GERD guidelines (ACG, ESGE, BSG). Evidence reviewed 2025.

Frequently Asked Questions

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