Gastro-oesophageal reflux disease (GORD) is a chronic condition where stomach acid returns into the oesophagus, causing symptoms like heartburn and acid regurgitation. It's often due to an incompetent lower oesophageal sphincter (LOS) or hiatus hernia. Management involves lifestyle changes, pharmacological acid suppression (PPIs), and occasionally surgery. Key complications include Barrett's oesophagus and oesophageal adenocarcinoma.
📋 Overview
Gastro-oesophageal reflux disease (GORD) is a very common presentation in UK primary care and a frequent topic in finals. It's defined by bothersome symptoms or complications from gastric content reflux into the oesophagus. The core issue is usually a dysfunctional lower oesophageal sphincter (LOS), allowing acid to reflux. Risk factors include obesity, pregnancy, hiatus hernia, smoking, and certain foods. Patients typically present with heartburn (retrosternal burning) and acid regurgitation, often worse after meals or when lying down. Crucially, recognise 'alarm symptoms' (dysphagia, weight loss, persistent vomiting, GI bleeding) which mandate urgent endoscopy (2-week wait referral) to rule out malignancy. Initial management is lifestyle modification. Pharmacological therapy starts with a full-dose Proton Pump Inhibitor (PPI) for 4-8 weeks. Long-term PPIs are used for persistent symptoms. Surgical options, like laparoscopic Nissen's fundoplication, are considered for refractory cases or those unable to tolerate long-term medication. Be aware of the link between GORD, Barrett's oesophagus, and oesophageal adenocarcinoma.
🔬 Basic Science
GORD pathophysiology centres on oesophageal mucosal exposure to acidic gastric juice (pH < 4). The main mechanism is transient lower oesophageal sphincter relaxations (TLOSRs), which occur independently of swallowing. A hypotensive LOS, delayed gastric emptying, and impaired oesophageal acid clearance also contribute. A hiatus hernia disrupts the normal anti-reflux barrier (angle of His, diaphragmatic crura) by allowing the stomach to protrude into the chest. Chronic acid exposure causes oesophagitis (inflammation). Persistent oesophagitis can lead to Barrett's oesophagus, where the normal stratified squamous epithelium of the distal oesophagus is replaced by specialised intestinal-type columnar epithelium with goblet cells. This metaplasia is a protective adaptation but carries a risk of progression through dysplasia to oesophageal adenocarcinoma. *H. pylori* infection's role is complex; eradication can sometimes worsen GORD symptoms by restoring normal gastric acid secretion.
🏥 Clinical Relevance
Classic presentation is retrosternal heartburn, often radiating upwards, exacerbated by bending, lifting, or lying flat. Patients may describe 'water brash' (sudden saliva surge) or acid regurgitation. Extra-oesophageal symptoms include chronic cough, hoarseness (reflux laryngitis), and dental erosions. Complications are important: peptic strictures cause progressive dysphagia (initially to solids), chronic oesophagitis can lead to iron deficiency anaemia, and Barrett's oesophagus increases the risk of oesophageal adenocarcinoma (0.1-0.5% annual risk). For finals, remember NICE NG12 criteria for urgent 2-week wait endoscopy: any dysphagia, or age 55+ with weight loss AND upper abdominal pain, reflux, or dyspepsia. Physical examination is usually normal. Key differentials include ischaemic heart disease (always exclude if chest pain is prominent), peptic ulcer disease, and eosinophilic oesophagitis.
🧪 Investigations
Bedside: BMI, vital signs. Bloods: FBC (check for anaemia), U&Es, LFTs. Imaging/Special tests: Upper GI Endoscopy (OGD) is the primary investigation. It assesses for oesophagitis (Los Angeles grades A-D), Barrett's, or malignancy. Biopsies are crucial if malignancy or Barrett's is suspected. 24-hour pH monitoring and oesophageal manometry are gold standard for diagnosing reflux but are usually reserved for pre-operative assessment or when the diagnosis is unclear despite OGD. *H. pylori* testing (urea breath test or stool antigen) is relevant if dyspepsia is a co-symptom.
💊 Management
Conservative: Lifestyle modifications are first-line: weight loss, smoking cessation, alcohol reduction, avoiding trigger foods (e.g., chocolate, fatty foods, caffeine), raising the head of the bed, and avoiding eating 3-4 hours before sleep. Medical: Full-dose PPI (e.g., Omeprazole 20mg OD or Lansoprazole 30mg OD) for 1 month. If successful, step down to lowest effective dose or 'as-needed'. If symptoms persist, consider doubling the PPI dose or adding an H2-receptor antagonist (e.g., Famotidine). Antacids and alginates (e.g., Gaviscon Advance) offer immediate, short-term relief. Surgical: Laparoscopic Nissen's fundoplication (wrapping the gastric fundus around the lower oesophagus) is indicated for severe, refractory symptoms or for patients who prefer surgery over lifelong medication.