GERD — Causes, Symptoms & Management Guide — Symptoms, Causes & Treatment | MyMedicPlus

Gastroesophageal Reflux Disease (GERD) is a chronic condition in which the lower esophageal sphincter (LES) — the muscular valve between the oesophagus and stomach — weakens or undergoes transient inappropriate relaxation, allowing gastric acid, pepsin, and bile to flow back (reflux) into the oesophagus and cause mucosal injury. GERD affects approximately 20% of adults in Western countries and 10–15% globally, making it one of the most prevalent gastrointestinal disorders worldwide. The Montreal Definition classifies GERD as the presence of troublesome symptoms or mucosal complications from gastric reflux at least twice per week. While heartburn (pyrosis) and regurgitation are the hallmark symptoms, GERD causes a wide spectrum of oesophageal complications — reflux oesophagitis, peptic stricture, Barrett's oesophagus (a pre-malignant mucosal metaplasia affecting 5–15% of patients), and ultimately oesophageal adenocarcinoma — as well as extra-oesophageal manifestations including chronic cough, laryngitis, and non-cardiac chest pain. Prompt diagnosis and sustained treatment significantly reduce complication risk.

The primary pathophysiological mechanism is inappropriate transient lower oesophageal sphincter relaxations (TLOSRs) — episodes of LES relaxation unrelated to swallowing, occurring spontaneously and allowing acid reflux without any propulsive action. Structural LES weakness is the second mechanism — reduced basal LES tone (normal: 10–35 mmHg) allows prolonged acid exposure. Hiatus hernia (herniation of the gastric cardia above the diaphragmatic hiatus) disrupts the oesophagogastric junction's anti-reflux mechanisms — the diaphragmatic crural pinch effect is lost, and the acid reservoir within the herniated gastric sac increases the frequency and duration of acid reflux episodes; hiatus hernia is present in 90% of patients with severe GERD and 50–60% of those with erosive oesophagitis. Delayed gastric emptying (gastroparesis — from diabetes, post-vagotomy, post-fundoplication) increases gastric reservoir pressure and promotes reflux. Dietary and lifestyle triggers: high-fat meals, coffee, chocolate, peppermint, alcohol, and tobacco all reduce LES pressure; large meal volumes increase gastric distension; carbonated drinks increase gastric pressure; recumbency within 3 hours of eating allows gravity-assisted reflux. Obesity and intra-abdominal hypertension: BMI above 30 increases GERD risk 3-fold — increased intra-abdominal pressure reduces the pressure gradient across the LES; waist circumference is a more accurate predictor of GERD risk than BMI alone. Medications that reduce LES tone and promote GERD: calcium channel blockers (amlodipine — commonly prescribed, reduces LES by 30–40%), nitrates, beta-agonists, aminophylline, anticholinergics, and opioids. Bile reflux (alkaline reflux) — bile and pancreatic secretions refluxing from the duodenum — contributes to mucosal injury, particularly in post-gastrectomy patients and those with combined acid-alkaline reflux.

Typical GERD symptoms — heartburn and regurgitation — are the most specific for the diagnosis: heartburn (pyrosis) is a retrosternal burning sensation rising from the epigastrium toward the throat, typically worsened by large meals, fatty food, supine position, stooping forward, and relieved (transiently) by antacids; present in over 90% of GERD patients. Acid regurgitation — effortless return of acid or bile-tasting fluid into the throat or mouth (unlike vomiting, it requires no retching effort) — is the second cardinal symptom; present in 70–80%. Atypical (extra-oesophageal) manifestations of GERD are increasingly recognised and include: chronic hoarseness or laryngitis (laryngopharyngeal reflux — LPR — posterior laryngeal erythema and pseudosulcus on laryngoscopy); chronic cough (GERD is one of the three most common causes of chronic cough in non-smokers, alongside post-nasal drip and asthma — micro-aspiration and vagal reflex bronchoconstriction); dental erosion (acid dissolves dental enamel); non-cardiac chest pain (GERD accounts for 50% of non-cardiac chest pain — oesophageal smooth muscle spasm or acid sensitisation of oesophageal pain receptors mimics angina); halitosis; and new-onset or worsening asthma. Alarm (red flag) symptoms that require urgent endoscopy to exclude malignancy: dysphagia (difficulty swallowing — suggests oesophageal stricture or cancer); odynophagia (painful swallowing); unintentional weight loss; haematemesis (vomiting blood) or melaena (black tarry stools); anaemia; and persistent vomiting. These symptoms are present in approximately 5% of GERD referrals but carry significant diagnostic yield for Barrett's oesophagus, peptic stricture, and oesophageal carcinoma.

GERD remains a clinical diagnosis in typical uncomplicated cases — symptom-based diagnosis using the Montreal Classification criteria (heartburn and/or regurgitation causing troublesome symptoms) has a positive predictive value of 65–78% against pH monitoring. Trial of PPI (proton pump inhibitor test): empirical PPI therapy (omeprazole 20–40 mg daily before breakfast for 4 weeks) — symptom improvement by 50% or more (the 'PPI test') has positive predictive value of 78% for GERD in patients with typical heartburn. Endoscopy (oesophago-gastro-duodenoscopy — OGD): the reference investigation for complications and alarm symptoms — assesses oesophageal mucosa for erosive oesophagitis (graded by Los Angeles Classification: Grade A = mucosal breaks confined to mucosal folds; Grade B = mucosal breaks longer than 5 mm; Grade C = mucosal breaks merging between folds; Grade D = mucosal breaks above 75% of circumference), Barrett's oesophagus (specialised intestinal metaplasia — diagnosed histologically from four-quadrant biopsies at 2 cm intervals of the Barrett's segment using the Seattle protocol; risk of oesophageal adenocarcinoma: 0.4–0.5% per year of non-dysplastic Barrett's; high-grade dysplasia — 5–6% per year), peptic stricture, and hiatus hernia. 24-hour pH impedance monitoring (catheter-based or wireless Bravo capsule): the gold standard for GERD diagnosis when endoscopy is normal and atypical symptoms persist despite PPI — records the frequency and duration of acid (pH below 4) and non-acid reflux events correlated with symptom episodes using the symptom index (SI) and symptom association probability (SAP); performed off PPI for 7 days to detect all reflux events. High-resolution oesophageal manometry (HRM): measures LES pressure, the oesophago-gastric junction (OGJ) integrated relaxation pressure, and oesophageal body peristaltic function — essential before any anti-reflux surgery to exclude major motility disorders (achalasia — which would cause catastrophic dysphagia post-fundoplication); the Chicago Classification v4.0 categorises motility disorders.

Proton pump inhibitors (PPIs) — omeprazole, lansoprazole, esomeprazole, pantoprazole, rabeprazole (the most effective acid-suppressive agents, inhibiting the H+/K+ ATPase proton pump irreversibly) — achieve 80–90% acid suppression when taken 30–60 minutes before the first meal of the day; standard dose: 4–8 weeks for initial treatment of erosive oesophagitis; the majority of patients require maintenance therapy for symptom control. H2 receptor antagonists (H2RAs — ranitidine — now withdrawn due to NDMA contamination concerns; famotidine, cimetidine, nizatidine): less potent than PPIs; used for mild symptoms or as add-on therapy for nocturnal breakthrough heartburn (famotidine 20 mg at bedtime). Potassium-competitive acid blockers (P-CABs — vonoprazan — approved in Japan and Asia; tegoprazan): faster onset than PPIs (do not require meal timing), maintain acid suppression at pH above 4 for longer durations — superior to PPIs for healing of severe (Grade C and D Los Angeles) erosive oesophagitis; increasingly used in H. pylori eradication regimens. Alginate therapy (Gaviscon Advance — sodium alginate + potassium bicarbonate): forms a viscous raft floating above the gastric contents, physically blocking reflux — particularly effective for post-prandial and nocturnal reflux; recommended as add-on therapy to PPIs for breakthrough symptoms. Anti-reflux surgery (laparoscopic Nissen fundoplication — 360° wrap of the gastric fundus around the oesophagus, restoring LES competence): indicated for documented pathological GERD with good PPI response (predicts symptom relief from surgery), young patients unwilling to take lifelong PPI, and those with objective large hiatus hernia; comparable long-term symptom control to medical management at 10 years; post-operative dysphagia in 10–15% (usually transient). Lifestyle modifications: weight loss (10% body weight loss reduces GERD severity by 40%); elevation of the bed head by 15–20 cm (or wedge pillow) for nocturnal symptoms; avoid lying flat for 3 hours after meals; smoking cessation.

Reflux esophagitis — erosion and inflammation of the esophageal mucosa — causes pain and bleeding. Peptic stricture from fibrosis causes progressive dysphagia requiring dilatation. Barrett's esophagus — metaplastic change of esophageal mucosa to intestinal-type epithelium — develops in approximately 5–15% of GERD patients and is a pre-malignant condition increasing esophageal adenocarcinoma risk 30–50 fold. Regular endoscopic surveillance every 3–5 years is recommended for Barrett's esophagus. Chronic aspiration from GERD can cause or worsen asthma, chronic cough, laryngitis, and recurrent pneumonia.

Achieve and maintain healthy body weight — each 5-unit BMI increase significantly worsens GERD symptoms and complication risk. Avoid trigger foods identified through a personal symptom diary. Elevate the head of the bed by 15–20 cm when experiencing nocturnal symptoms. Eat smaller meals and avoid eating within 3 hours of bedtime. Quit smoking — smoking reduces LES tone and worsens esophageal acid clearance. Take PPIs consistently as prescribed: do not stop abruptly as rebound acid hypersecretion can occur. If on long-term PPI therapy (more than 1 year), ensure adequate calcium and magnesium intake as PPIs may reduce their absorption.

Seek emergency care for: sudden severe chest pain or pressure (to exclude heart attack before attributing to GERD), difficulty or painful swallowing (dysphagia — may indicate oesophageal stricture or cancer), vomiting blood (haematemesis), or black tarry stools (melaena — GI bleeding). See your GP promptly for: heartburn persisting more than 3 weeks despite antacids, new onset of dysphagia (particularly to solids — red flag for oesophageal cancer), unexplained weight loss, anaemia, regurgitation of blood or old food, or GERD symptoms in anyone over 55 with new onset or worsening symptoms. Refer for urgent endoscopy (OGD) for alarm symptoms. See a gastroenterologist for: GERD not responding to PPI therapy, consideration of Barrett's oesophagus surveillance, pre-operative assessment for antireflux surgery.