Esophagitis

• Esophagitis: This is the swelling of the esophagus lining, usually resulting from direct damage to the mucosa or due to systemic inflammatory disorders.
• Eosinophilic Esophagitis: A chronic condition where the esophagus lining is inflamed due to immune system activity, primarily involving eosinophils, a type of white blood cell.
• Infectious Esophagitis: This form of esophagitis is caused by infections and is most commonly seen in individuals with weakened immune systems.
• Substance-Induced Esophagitis: Occurs when the esophagus lining is irritated by direct contact with harmful substances.
• Medication-Induced Esophagitis: A specific type of substance-induced esophagitis, this occurs when certain oral medications, like antibiotics, anti-inflammatory drugs, or bisphosphonates, linger and damage the esophagus lining.

• Mucosal injury
  • Gastroesophageal reflux disease (GERD)
  • Infections (Candida spp., Herpes simplex virus (HSV), Cytomegalovirus (CMV))
  • Substance-induced esophagitis
  • Radiotherapy
• Eosinophilic esophagitis
• Lymphocytic esophagitis
• Immune-mediated disorders (Crohn disease, scleroderma, Behcet disease, systemic lupus erythematosus, Sjogren syndrome)
• Motility disorders (e.g., achalasia, muscular dystrophy)

• Heartburn
• May be associated with dyspepsia, regurgitation, belching, and globus sensation
• Features of the underlying etiology
  • Heartburn that worsens on lying down or bending forward: GERD
  • Retrosternal chest pain, dysphagia, and reflux of undigested food particles: achalasia cardia
  • Dysphagia, weight loss, hematemesis: esophageal cancer

Clinical features

• Odynophagia, dysphagia (most characteristic)
• Heartburn, regurgitation
• Mouth ulcers and thrush
• Retrosternal chest pain
• Systemic signs of infection (e.g., fever)

Etiology

• Fungal: Candida spp. (most common cause is Candida albican. Candida glabrata andCandida krusei are less common)
• Viral: CMV, HSV (HSV-1)

Diagnostics and treatment

Etiology

• Allergic disorder associated with:
  • Antigen sensitization through foods or aeroallergens
  • Eosinophilia and esophageal dysfunction
• Note: Eosinophils are not normally found in the esophagus.

Pathophysiology

• Eosinophils are recruited on exposure to inhaled or congested allergens.
• Eosinophilic infiltration occurs → eosinophils release interleukins → inflammatory response

Clinical features

• Dysphagia (to solid foods)
• Food impaction
• Odynophagia
• Symptoms can be worsened by ingestion of food containing allergens.
• Associated features: atopy (e.g., asthma, rhinitis, atopic dermatitis, alimentary allergies)

Diagnosis

Diagnosis is done by upper endoscopy.

• Mucosal rings in the esophagus
• Biopsy showing eosinophils (> 15/HPF (high-power field))
• Other features:
  • Esophageal eosinophilia persists even with proton pump inhibitor (PPI) intake.
  • Normal pH monitoring

Treatment

• Dietary elimination (avoiding allergens): Exclude certain protein groups (e.g., milk, soy, nuts) from the diet to reduce the inflammatory response in the GI tract.
• Topical glucocorticoids (e.g., swallowed fluticasone or Budesonide)
• Systemic glucocorticoids if with significant dysphagia, weight loss, dehydration
• PPI for reflux symptoms

Etiology: direct mucosal injury caused by prolonged contact with a certain drug

• Antibiotics (e.g., tetracycline, doxycycline, and clindamycin)
• Antiinflammatory drugs, NSAIDs, aspirin
• Bisphosphonates (e.g., alendronate)
• Others (e.g., potassium chloride, iron compounds, quinidine)

Diagnosis

• Clinical diagnosis based on history
• Upper endoscopy:
  • Perform if with severe or persistent symptoms (despite discontinuation of the offending medication)
  • Findings: discrete ulcer, with normal bordering mucosa

Treatment: Most cases are self-limiting.

• Discontinue the medication or substance causing esophagitis.
• Ensure nutrition and hydration (Some patients may require IV fluids until PO is tolerable).
• Consider antacids, sucralfate, or PPIs to ameliorate symptoms.
  • If medication is necessary, take the medication with enough water and maintain an upright position for at least 30 minutes.
• Some patients may develop strictures that require esophageal dilations.

Etiology

• Alkali:
  • Drain cleaners, household cleaning products, batteries, bleaches
  • Viscous, tasteless, colorless
• Acids:
  • Battery fluid, toilet bowl cleaners, metal-cleaning liquids, anti-rust solutions
  • Unpleasant taste, malodorous

Pathophysiology

• Alkali-induced injury:
  • Rapid damage, affecting esophagus more than the stomach
  • Large amounts, however, result in gastric injury.
  • Process: liquefactive necrosis in the esophagus
• Acid-induced injury:
  • Pain on contact with the oropharynx limits the amount ingested.
  • More oropharyngeal and airway damage than with alkali solutions
  • Acid passes down faster, causing more stomach damage.
  • Process: superficial coagulation necrosis in the esophagus

Diagnosis

• History: Note type and amount of ingested agent.
• X-rays:
  • Chest: check for pneumomediastinum, aspiration pneumonia, foreign body (e.g., battery)
  • Abdominal: check for pneumoperitoneum, foreign body
  • Computed tomography (CT) scan: checks depth of necrosis and helps assess need for emergency surgery
• Upper endoscopy:
  • Within 24 hours if without contraindications
  • Contraindicated in hemodynamic instability, gastrointestinal perforation

Classification of injury

• 1st-degree injury: superficial mucosa affected; erythema, edema, hemorrhage, with healing expected
• 2nd-degree injury: ulcers, exudates affect up to submucosal layer; scarring and strictures possible
• 3rd-degree injury: transmural in-depth, with deep ulcers and perforation of the wall

Management

• Airway protection; assess need for intubation
• Fluid resuscitation
• NPO (nothing by mouth)
• No nasogastric insertion, no emetics
• PPIs
• Antibiotics for suspected perforation
• Evaluate for surgical indications
• Surveillance: upper endoscopy 15–20 years later to screen for SCC