Acid Reflux & GERD — Causes, Symptoms & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Gastroesophageal reflux disease (GERD) is a chronic digestive disorder in which stomach acid repeatedly flows back through the lower esophageal sphincter (LES) into the esophagus, causing mucosal irritation, inflammation, and over time structural damage. GERD is one of the most prevalent gastrointestinal conditions globally, affecting approximately 20% of adults in Western countries and up to 10-15% in Asia — with incidence rising worldwide. The condition is defined clinically by troublesome symptoms (heartburn, regurgitation) occurring at least twice weekly, or by documented mucosal complications. The pathophysiology centres on inappropriate transient LES relaxations, reduced LES resting tone aggravated by obesity, pregnancy, and hiatal hernia, impaired esophageal acid clearance, and increased intra-abdominal pressure. Hiatal hernia — present in approximately 50% of GERD patients — allows the stomach to herniate through the diaphragm, disrupting the gastro-esophageal junction and the normal anti-reflux barrier. Prolonged acid exposure causes progressive mucosal injury — from mild esophagitis to Barrett's metaplasia and, in some cases, esophageal adenocarcinoma. GERD significantly impairs quality of life, with frequent heartburn associated with sleep disturbance, reduced productivity, and anxiety.

GERD results from a weakened or inappropriately relaxing lower esophageal sphincter (LES), allowing gastric contents to reflux into the esophagus. The primary mechanism is transient LES relaxation — brief episodes unrelated to swallowing, triggered by gastric distension. Structural risk factors: hiatal hernia (present in 50% of GERD cases), obesity (BMI above 30 increases GERD risk 2-fold by increasing intra-abdominal pressure), and pregnancy (progesterone reduces LES tone). Medications that reduce LES pressure include calcium channel blockers (amlodipine), anticholinergics, benzodiazepines, opioids, nitrates, and NSAIDs (which also directly damage the gastric and esophageal mucosa). Common dietary triggers: fatty or fried foods, coffee, caffeinated drinks, alcohol, chocolate, peppermint, citrus fruits, and tomato-based products. Lifestyle risk factors: cigarette smoking reduces LES pressure and impairs esophageal mucosal defences; eating large meals; lying down within 2-3 hours of eating; eating very rapidly; and tight abdominal clothing or belts that increase intra-abdominal pressure.

The cardinal symptom of GERD is heartburn — a burning retrosternal discomfort typically occurring 30-60 minutes after meals, provoked by bending forward, lying down, or trigger foods, and relieved by antacids or upright position. Regurgitation — effortless return of sour or bitter gastric contents into the mouth or throat — is the second hallmark symptom. Atypical or extraesophageal manifestations include chronic dry cough (acid microaspiration stimulates the cough reflex — present in up to 40% of GERD patients), hoarseness or dysphonia from acid laryngitis, globus sensation (persistent lump-in-the-throat feeling), dental erosion (acid dissolves posterior tooth enamel), and asthma exacerbation (GERD is present in 40-80% of asthmatic patients). Dysphagia (difficulty swallowing solid food) suggests esophageal stricture or Barrett's esophagus and requires urgent endoscopic evaluation. Odynophagia (painful swallowing) indicates severe ulcerative esophagitis. GERD can cause severe chest pressure indistinguishable from cardiac angina — cardiac causes must always be excluded first before attributing chest pain to reflux.

GERD is primarily a clinical diagnosis — the combination of typical heartburn and regurgitation responding to a 4-8 week empirical proton pump inhibitor (PPI) trial is sufficient to confirm the diagnosis in most patients without alarm symptoms. Upper endoscopy (gastroscopy) is indicated for: alarm symptoms (dysphagia, unintentional weight loss, anaemia, haematemesis, persistent vomiting), age above 55 with new-onset symptoms, or failure to respond to 8 weeks of PPI therapy — it grades oesophagitis by the Los Angeles (LA) Classification (Grade A-D) and detects peptic stricture, Barrett's oesophagus, or malignancy. Ambulatory 24-hour pH monitoring or wireless pH capsule (Bravo) measures oesophageal acid exposure time (abnormal above 4-6%) and is the gold standard for confirming pathological acid reflux in patients with normal endoscopy or atypical symptoms. Combined impedance-pH monitoring additionally detects non-acid and weakly-acidic reflux. High-resolution oesophageal manometry assesses LES pressure and oesophageal motility — essential before anti-reflux surgery to exclude achalasia. Barium swallow detects hiatal hernia, peptic stricture, and oesophageal dysmotility.

Treatment of GERD is stepwise, combining lifestyle modification with pharmacological and, when indicated, surgical therapy. Lifestyle: weight loss of even 5-10% body weight substantially reduces GERD symptom frequency in overweight patients; elevating the bed head 15-20 cm with a wedge pillow or bed risers reduces nocturnal reflux; avoiding eating within 2-3 hours of bedtime; eliminating trigger foods and alcohol; and quitting smoking. Antacids (calcium carbonate, magnesium hydroxide) and alginate preparations (Gaviscon) provide rapid symptom relief for mild intermittent heartburn. H2-receptor antagonists (famotidine) reduce acid secretion and work faster than PPIs — useful for on-demand or nocturnal breakthrough symptoms. Proton pump inhibitors (PPIs) are the most effective medical therapy: omeprazole 20 mg, pantoprazole 40 mg, lansoprazole 30 mg, or esomeprazole 40 mg taken 30-60 minutes before breakfast daily — healing esophagitis in 80-90% of patients within 8 weeks. PPIs are used at the lowest effective dose for the shortest necessary duration; Step-down to on-demand PPI is appropriate for symptom control in non-erosive GERD. For refractory GERD, switching PPI, twice-daily dosing, or adding baclofen (GABA-B agonist that reduces transient LES relaxations) may help. Anti-reflux surgery: laparoscopic Nissen fundoplication (360-degree gastric wrap around the LES) is equally effective to PPI therapy for regurgitation-predominant GERD in suitable candidates. LINX magnetic sphincter augmentation is a newer minimally invasive alternative. Surgery is preferred for young patients with large hiatal hernia or those seeking to avoid lifelong medication.

Chronic untreated GERD causes progressive esophageal mucosal injury with serious long-term consequences. Erosive oesophagitis causes bleeding, iron deficiency anaemia, and haematemesis. Peptic stricture — fibrotic narrowing of the oesophageal lumen from chronic acid-induced scarring — occurs in approximately 10% of patients with long-standing severe oesophagitis, causing progressive solid food dysphagia requiring endoscopic balloon dilatation. Barrett's oesophagus — intestinal metaplasia of the squamous oesophageal epithelium — develops in 10-15% of GERD patients after years of acid exposure and is a premalignant condition carrying a 30-40-fold increased risk of oesophageal adenocarcinoma. Oesophageal adenocarcinoma is one of the fastest-rising cancers in Western countries (7-fold rise in incidence over 40 years) with a 5-year survival below 20% in advanced stages; surveillance endoscopy and ablation of dysplastic Barrett's tissue (radiofrequency ablation, endoscopic mucosal resection) can prevent progression. Chronic acid microaspiration causes laryngeal damage (vocal cord granulomas and subglottic stenosis), worsens asthma, and in the elderly can precipitate aspiration pneumonia and respiratory failure.

Maintain a healthy weight — even 5-10% weight reduction in overweight individuals substantially reduces GERD symptom frequency and severity. Avoid known dietary triggers (fatty foods, coffee, alcohol, chocolate, peppermint, citrus, spicy foods) and eat smaller, more frequent meals rather than large meals. Do not lie down for at least 2-3 hours after eating; avoid late-night snacks. Elevate the head of the bed by 15-20 cm using a wedge pillow or bed risers — this uses gravity to reduce nocturnal reflux and is one of the most effective non-pharmacological measures. Quit smoking — nicotine reduces LES tone and impairs oesophageal mucosal defences. Limit alcohol, particularly wine and beer. Avoid tight waistbands and abdominal compression. Review medications that may worsen reflux (NSAIDs, calcium channel blockers, nitrates, benzodiazepines) with your doctor. Regular endoscopic surveillance every 3-5 years — or annual surveillance with dysplasia — is essential for all patients with confirmed Barrett's oesophagus to detect and treat premalignant changes before cancer develops.

Go to an emergency department immediately for: severe chest pain that could indicate a heart attack (GERD can mimic cardiac pain — if uncertain, seek emergency care); difficulty swallowing that is progressive or associated with weight loss (possible stricture or malignancy); vomiting blood or passing black tarry stools (upper GI bleeding — complication of severe oesophagitis or peptic ulcer). See your GP urgently for: persistent heartburn despite 2-4 weeks of over-the-counter antacids or H2 blockers; new or worsening heartburn in anyone over 55; frequent symptoms (twice per week or more) — GERD requires medical evaluation and monitoring for Barrett's oesophagus; and unintentional weight loss combined with swallowing difficulty or heartburn. Regular endoscopic surveillance every 3-5 years is essential for patients with confirmed Barrett's oesophagus to detect dysplasia before it progresses to cancer.