GERD / Acid Reflux: Managing Heartburn and Oesophageal Damage

Dietary Triggers

Management Ladder

1. Lifestyle: elevate bed head 15–20 cm; avoid triggers; lose weight (strongly linked); eat smaller meals; don't lie down for 3 hours after eating
2. Antacids (Gaviscon, Rennies): neutralise acid; symptom relief only
3. H2 blockers (famotidine, ranitidine): reduce acid for mild GERD
4. PPIs (omeprazole, lansoprazole, esomeprazole): most effective acid suppression; use lowest effective dose; consider step-down after 8 weeks
5. Laparoscopic fundoplication: surgical option for refractory GERD or those refusing lifelong PPIs

References

The clinical information on this page is drawn from peer-reviewed sources indexed by the US National Library of Medicine. Links go to the source so you can read it yourself.

1. Gastroesophageal Reflux Disease (GERD). In: StatPearls. Treasure Island (FL): StatPearls Publishing. NCBI Bookshelf NBK554462

References

Sources cited on this page. PubMed links open the original abstract.

1. Katz PO, Gerson LB, Vela MF. Guidelines for the diagnosis and management of gastroesophageal reflux disease. Am J Gastroenterol. 2013;108(3):308–328. PMID 23419381 · doi:10.1038/ajg.2012.444

The acid-pepsin mechanism and why GERD differs from GORD

Gastro-oesophageal reflux disease (GORD in the UK; GERD in the USA) occurs when stomach acid – and sometimes bile and pepsin – refluxes into the oesophagus. The lower oesophageal sphincter (LOS) normally maintains a pressure barrier preventing this; GERD results from LOS dysfunction (reduced resting pressure or transient relaxations), increased intra-abdominal pressure (obesity, pregnancy), or impaired oesophageal clearance.

The oesophagus lacks the protective mucus layer of the stomach. Repeated acid exposure causes:

• Oesophagitis – inflammation and mucosal erosion (Los Angeles grade A–D)
• Stricture formation – scarring causing dysphagia (difficulty swallowing)
• Barrett's oesophagus – the most important complication: intestinal metaplasia (stomach-type columnar epithelium replacing normal squamous cells), a pre-malignant condition conferring a 0.2–0.5% annual risk of developing oesophageal adenocarcinoma

When to investigate beyond symptoms – alarm features requiring endoscopy

NICE guidelines (NG12) recommend urgent upper GI endoscopy (within 2 weeks) for reflux symptoms accompanied by any of these alarm features:

• Dysphagia (difficulty swallowing) – could indicate stricture or cancer
• Odynophagia (painful swallowing)
• Unintentional weight loss
• Vomiting with blood or coffee-ground material (haematemesis)
• Iron deficiency anaemia
• New reflux or dyspepsia after age 55

Routine blood tests are not diagnostic for GERD but help exclude contributing conditions: FBC for iron deficiency anaemia (suggesting occult upper GI bleeding); H. pylori testing (urea breath test or stool antigen test – H. pylori causes peptic ulcer disease that worsens reflux symptoms); and coeliac serology (coeliac disease impairs gastric motility and increases reflux).

Barrett's oesophagus – surveillance and risk reduction

Once Barrett's oesophagus is confirmed on endoscopy with biopsy, NICE recommends endoscopic surveillance to detect dysplasia early. Frequency depends on Barrett's segment length: non-dysplastic short-segment Barrett's may be surveilled every 3–5 years; high-grade dysplasia requires endoscopic eradication therapy (radiofrequency ablation or endoscopic mucosal resection) rather than surgery. Patients with confirmed Barrett's should take long-term high-dose PPI therapy regardless of symptom control, as acid suppression may slow dysplasia progression.