Reflux Esophagitis

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Reflux Esophagitis 


1. Definition

Reflux esophagitis is a condition in which the reflux of gastric contents into the esophagus causes mucosal injury. This occurs as aggressive substances such as gastric acid, pepsin, and sometimes bile repeatedly come into contact with the esophageal lining, leading to inflammation.


2. Cause and Etiology

The primary cause of reflux esophagitis is dysfunction of the lower esophageal sphincter (LES). When transient lower esophageal sphincter relaxations (TLESRs) occur frequently, or when the resting LES pressure is reduced, gastric acid can reflux into the esophagus more easily. Anatomical abnormalities such as hiatal hernia can also impair LES function, promoting reflux.

Impaired esophageal acid clearance or reduced salivary secretion prolongs acid exposure in the esophagus, increasing mucosal injury. Delayed gastric emptying and excessive gastric content accumulation elevate intragastric pressure, facilitating reflux. Contributing factors include high-fat diets, alcohol, caffeine, smoking, obesity, and pregnancy, all of which either lower LES tone or increase intra-abdominal pressure.


3. Pathophysiology

The fundamental pathophysiology involves direct chemical injury to the esophageal mucosa by gastric acid and pepsin. Acid causes cellular dehydration and necrosis, while pepsin breaks down mucosal proteins, impairing the protective barrier. Bile reflux can further exacerbate mucosal damage.

Inflammatory mediators such as IL-1, IL-6, and TNF-α are elevated, activating NF-κB and MAPK pathways that amplify tissue injury. Chronic inflammation induces histopathologic changes including basal cell hyperplasia, elongation of the lamina propria papillae, and dilation of intercellular spaces. Persistent damage and repair cycles can lead to fibrosis, resulting in complications such as strictures, ulcers, and Barrett’s esophagus.


4. Epidemiology

Reflux esophagitis is increasingly prevalent worldwide. In Western countries, approximately 20–30% of the general population experience GERD symptoms, and among them, a significant portion exhibit endoscopic evidence of esophagitis. In Eastern populations, the incidence has historically been lower, but it is rising due to Westernized diets, increasing obesity, and declining Helicobacter pylori infection rates.

Risk factors include obesity, aging, male sex, smoking, alcohol consumption, hiatal hernia, and the use of certain medications. Abdominal obesity, in particular, elevates intra-gastric pressure, predisposing to reflux.


5. Clinical Presentation

The hallmark symptoms of reflux esophagitis are heartburn and acid regurgitation. These symptoms typically worsen after meals or when lying down, and patients often report a sour or bitter taste rising into the mouth.

Atypical symptoms include chronic cough, sore throat, hoarseness, recurrent laryngitis, exacerbation of asthma, and dental erosion. These may be misinterpreted as upper airway diseases, potentially delaying diagnosis.

Alarm symptoms include dysphagia, odynophagia, weight loss, bleeding (hematemesis or melena), and anemia, all of which necessitate prompt endoscopic evaluation.


6. Diagnosis and Imaging Findings

Diagnosis of reflux esophagitis is primarily made via upper gastrointestinal endoscopy. Typical endoscopic findings include mucosal erythema, erosions, ulcers, and exudates. The severity is classified using the Los Angeles classification system.


Biopsies may be taken to rule out Barrett’s esophagus, esophageal carcinoma, or eosinophilic esophagitis. Ambulatory 24-hour pH monitoring or combined impedance-pH monitoring may be used to confirm acid or non-acid reflux. High-resolution esophageal manometry assesses LES function and esophageal motility, particularly before surgery. Barium swallow studies can help detect anatomical abnormalities such as strictures or hiatal hernias.


7. Treatment

Management of reflux esophagitis includes lifestyle modification, pharmacologic therapy, and surgical intervention.

Lifestyle changes include weight loss, avoiding lying down after meals, dietary adjustments (avoiding trigger foods such as caffeine, chocolate, spicy foods), smoking cessation, and alcohol moderation. Elevating the head of the bed and maintaining an upright position post-meal are also recommended.

Pharmacologic treatment starts with proton pump inhibitors (PPIs), which effectively reduce gastric acid secretion and promote mucosal healing. Common agents include omeprazole, esomeprazole, and pantoprazole. Recently, potassium-competitive acid blockers (P-CABs) like vonoprazan have shown superior acid suppression and are especially effective in severe cases.

In cases of delayed gastric emptying, prokinetic agents such as metoclopramide or domperidone may be added. Alginates may be used to form a mechanical barrier and reduce acid contact with the mucosa.

Patients who fail medical therapy or develop complications may be candidates for anti-reflux surgery such as Nissen fundoplication, magnetic sphincter augmentation (LINX), or endoscopic therapies including Stretta and transoral incisionless fundoplication (TIF).


8. Complications

Complications of reflux esophagitis include esophageal ulcers, bleeding, peptic strictures, and Barrett’s esophagus. Barrett’s esophagus is a metaplastic transformation from normal squamous epithelium to intestinal-type columnar epithelium and is a known precursor to esophageal adenocarcinoma.

Strictures occur due to fibrotic healing of repeated ulceration, leading to progressive dysphagia. Long-standing inflammation increases the risk of malignant transformation, particularly in those with Barrett’s esophagus.


9. Prognosis

Mild to moderate reflux esophagitis typically responds well to PPI therapy, with mucosal healing observed within 4 to 8 weeks in most cases. However, recurrence is common if lifestyle modifications are not maintained or if medication adherence is poor.

In patients with Barrett’s esophagus, regular endoscopic surveillance is recommended due to the risk of dysplasia and progression to cancer. High-grade dysplasia may warrant endoscopic resection or ablation therapy.

Long-term PPI use necessitates monitoring for potential side effects, including hypomagnesemia, vitamin B12 deficiency, osteoporosis, and renal dysfunction. Nevertheless, with appropriate management, most patients experience significant symptom relief and mucosal healing.


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