Reflux Esophagitis: Causes, Pathophysiology, Imaging Features, Treatment, and Prognosis

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Introduction

Reflux esophagitis, a common manifestation of gastroesophageal reflux disease (GERD), is one of the most frequent inflammatory disorders of the esophagus. It results from the backflow of gastric or duodenal contents into the esophagus due to dysfunction of the lower esophageal sphincter (LES). Chronic reflux leads not only to mucosal inflammation but also to complications such as esophageal strictures, Barrett’s esophagus, and esophageal adenocarcinoma.

This column provides a comprehensive expert-level review of reflux esophagitis with detailed explanations of its cause, etiology, pathophysiology, epidemiology, clinical presentation, imaging features, treatment, and prognosis, supported by radiologic findings and evidence-based data.

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Cause and Etiology of Reflux Esophagitis

The primary cause of reflux esophagitis is LES dysfunction, which fails to prevent the retrograde movement of gastric or duodenal contents into the esophagus.

  • LES Dysfunction: Normally, the LES acts as a barrier preventing reflux. Dysfunction occurs when the sphincter has low resting tone or transient inappropriate relaxation.

  • Hiatal Hernia: A structural abnormality where part of the stomach herniates into the thoracic cavity, impairing LES function.

  • Achalasia and Scleroderma: Neuromuscular disorders affecting esophageal motility and sphincter control.

  • Chemical Injury: Exposure to gastric acid, pepsin, bile, and pancreatic enzymes injures the squamous epithelium.

Thus, multifactorial etiology involving mechanical (hiatal hernia), neuromuscular (achalasia), and biochemical (acid/pepsin reflux) mechanisms contributes to disease onset.

Pathophysiology

The pathophysiology of reflux esophagitis is centered around mucosal injury caused by acid-peptic reflux:

  1. Chemical Irritation: Gastric acid and pepsin disrupt intercellular junctions, increasing mucosal permeability.

  2. Inflammation Cascade: Chronic acid exposure activates cytokines (IL-6, TNF-α), leading to inflammation, ulceration, and fibrosis.

  3. Neural Damage: Damage to Auerbach’s plexus impairs esophageal motility.

  4. Barrett’s Metaplasia: Prolonged injury causes squamous-to-columnar epithelial transformation, predisposing to adenocarcinoma.

Epidemiology

  • GERD affects 15–30% of the global population.

  • Reflux esophagitis occurs in approximately 20–40% of GERD patients.

  • Risk factors include obesity, smoking, alcohol, pregnancy, certain medications (NSAIDs, calcium channel blockers), and diets high in fat or caffeine.

  • Barrett’s esophagus occurs in 10–15% of chronic reflux patients and increases the risk of esophageal adenocarcinoma by up to 30-fold.

Clinical Presentation

Typical symptoms include:

  • Heartburn (pyrosis): Retrosternal burning, worse when lying down.

  • Regurgitation: Perception of acid reflux into the throat/mouth.

  • Dysphagia: Progressive difficulty in swallowing, especially with solid foods.

  • Chest Pain: Non-cardiac pain mimicking angina.

Complications may present as:

  • Esophageal Strictures: Progressive dysphagia.

  • Barrett’s Esophagus: Often asymptomatic, but detected during surveillance endoscopy.

  • Respiratory Symptoms: Cough, asthma exacerbation, aspiration pneumonia.

Imaging Features

Radiological assessment is critical for diagnosis and complications.

1. Double-contrast Barium Esophagography

  • More sensitive (~90%) than single-contrast studies for reflux esophagitis.

  • Findings include:

    • Abnormal Motility: Weak or absent peristalsis with non-peristaltic contractions.

    • Mucosal Nodularity: Granular/nodular mucosa in early disease.

    • Ulcers: Small barium collections near the gastroesophageal junction.

    • Thickened Folds: Indicative of edema/inflammation.

    • Strictures: Smooth concentric narrowing, often above a hiatal hernia.

2. Endoscopy

  • Gold standard for detecting mucosal injury.

  • Identifies erosions, ulcers, strictures, and Barrett’s mucosa.

3. pH Monitoring & Manometry

  • pH <4 for >5% of monitoring time indicates significant acid reflux.

  • Manometry assesses LES pressure and esophageal motility.

Barrett’s Esophagus

A serious complication of reflux esophagitis is characterized by metaplastic replacement of squamous epithelium with columnar epithelium.

  • Radiographic features:

    • High esophageal strictures.

    • Deep penetrating ulcers.

    • Reticular mucosal pattern.

  • Endoscopy with biopsy confirms diagnosis.

Figure 1. Barium swallow in a patient with Barrett’s esophagus. The arrow indicates the new squamo-columnar junction. Note mucosal irregularity below the transition point.


Treatment

1. Lifestyle Modification

  • Weight reduction, head-of-bed elevation, avoidance of alcohol, smoking, caffeine, and late-night meals.

2. Pharmacologic Therapy

  • Proton Pump Inhibitors (PPIs): First-line, effective in >90% of cases.

  • H2 Receptor Antagonists: Alternative for mild cases.

  • Prokinetics (Metoclopramide, Domperidone): Improve gastric emptying.

  • Antacids: For symptomatic relief.

3. Endoscopic and Surgical Therapy

  • Endoscopic therapies: Radiofrequency ablation, endoscopic mucosal resection for Barrett’s dysplasia.

  • Nissen Fundoplication: Gold standard surgical treatment for refractory GERD.

Prognosis

  • Mild reflux esophagitis responds well to medical therapy.

  • Strictures may require dilation or stenting.

  • Barrett’s esophagus necessitates lifelong surveillance due to adenocarcinoma risk.

  • Esophageal adenocarcinoma has a poor prognosis unless detected early.

Overall, prognosis is excellent with early diagnosis and treatment, but delayed management increases the risks of stricture formation and malignancy.

Quiz

1. Which of the following is NOT a typical complication of reflux esophagitis?

  1. Esophageal stricture

  2. Barrett’s esophagus

  3. Esophageal adenocarcinoma

  4. Crohn’s disease


2. Which radiological finding is most characteristic of reflux esophagitis?

  1. Bird-beak sign

  2. Mucosal nodularity and thickened folds

  3. Apple-core lesion

  4. String sign


Answer & Explanation

1. Answer: 4. Crohn’s disease. Explanation: Crohn’s disease is an inflammatory bowel disease unrelated to reflux esophagitis. The others are well-established complications.

2. Answer: 2. Mucosal nodularity and thickened folds. Explanation: These findings on barium swallow suggest mucosal inflammation and edema typical of reflux esophagitis. Bird-beak (achalasia), apple-core (colon carcinoma), and string sign (Crohn’s disease) are not related.

Conclusion

Reflux esophagitis represents a common yet potentially serious condition with a spectrum ranging from mild inflammation to Barrett’s esophagus and adenocarcinoma. Recognition of clinical features, imaging findings, and early intervention with lifestyle modification and pharmacologic therapy are essential to prevent progression.

Advanced cases require endoscopic or surgical treatment and long-term surveillance. With growing prevalence worldwide, particularly in Western and Asian populations, reflux esophagitis remains a major healthcare concern.

References

[1] J. E. Richter and D. O. Castell, "Gastroesophageal reflux disease: pathogenesis, diagnosis, and therapy," Annals of Internal Medicine, vol. 117, no. 11, pp. 937–947, 1992.
[2] J. Vakil et al., "The Montreal definition and classification of gastroesophageal reflux disease: a global evidence-based consensus," Am J Gastroenterol, vol. 101, no. 8, pp. 1900–1920, 2006.
[3] P. Sharma et al., "Barrett’s esophagus: epidemiology, diagnosis, and clinical management," Ann Rev Med, vol. 60, pp. 221–236, 2009.
[4] D. Y. Graham, "Pathogenesis of reflux esophagitis," Gastroenterology Clinics of North America, vol. 19, no. 3, pp. 683–703, 1990.
[5] J. Dent et al., "Epidemiology of gastro-oesophageal reflux disease: a systematic review," Gut, vol. 54, no. 5, pp. 710–717, 2005.
[6] R. Fass and S. Shapiro, "Systematic review: proton-pump inhibitor failure in gastro-oesophageal reflux disease—where next?" Aliment Pharmacol Ther, vol. 22, pp. 79–94, 2005.
[7] S. Spechler, "Clinical practice: Barrett’s esophagus," New England Journal of Medicine, vol. 346, no. 11, pp. 836–842, 2002.

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