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Diseases and Injuries of the Esophagus

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1. Classification of Esophageal Diseases

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2. Methods for Diagnosing Esophageal Diseases

Clinical Assessment

• History: dysphagia (solid vs. liquid), odynophagia, heartburn, regurgitation, chest pain, weight loss
• Dysphagia to solids → mechanical obstruction; to solids + liquids from onset → motility disorder

Imaging

• Barium swallow (esophagram): First-line for structural lesions, strictures, diverticula, rings. Excellent for Zenker diverticula and achalasia (classic "bird-beak" deformity at the LES). Also useful after food disimpaction.
• Plain radiograph / CT: Localization of radio-opaque foreign bodies; detection of free air (perforation), pneumomediastinum.
• CT chest/abdomen: Assessment of esophageal wall, surrounding structures, staging malignancy.

Endoscopy (EGD)

• Gold standard for mucosal evaluation: esophagitis, Barrett esophagus, malignancy, strictures, varices.
• Allows biopsy and therapeutic intervention (dilation, foreign body removal, hemostasis).
• For caustic burns: grading of injury within 12–48 hours of ingestion.

Manometry

• High-Resolution Manometry (HRM): Most precise tool for motility disorders. Maps pressure along entire esophagus including upper and lower esophageal sphincters. Classifies achalasia into three subtypes. Mandatory before surgical intervention (Heller myotomy) and essential in evaluating epiphrenic diverticula for associated motility disorders. — Sleisenger and Fordtran's

pH Monitoring

• 24-hour ambulatory pH monitoring / pH-impedance: Quantifies acid (and non-acid) reflux episodes, correlates symptoms with reflux events. Used when GERD symptoms persist despite therapy or before anti-reflux surgery.

Additional

• Endoscopic ultrasound (EUS): Staging esophageal malignancy, assessing submucosal lesions.
• Nuclear scintigraphy: Esophageal transit studies in motility disorders.

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3. Complications of Gastroesophageal Reflux (GERD)

(a) Mucosal Complications

• Reflux esophagitis: Mucosal injury from acid + pepsin (most damaging combination). Bile acids and pancreatic enzymes from duodenal reflux further potentiate injury.
• Peptic stricture: Chronic esophagitis → fibrosis → luminal narrowing. Presents with progressive dysphagia to solids. Managed with dilation and PPI therapy.
• Esophageal ulceration: Deep ulcers may cause bleeding or perforation.

(b) Respiratory / Extraesophageal Complications

• Asthma: 35–50% of asthmatics have abnormal esophageal pH, esophagitis, or hiatal hernia. Reflux triggers bronchospasm by microaspiration and vagally mediated reflexes.
• Chronic cough: A major extraesophageal manifestation.
• Laryngitis / hoarseness, dental erosions, sinusitis.
• Idiopathic pulmonary fibrosis (IPF): Association with chronic microaspiration.
• COPD exacerbations: Patients with GERD are twice as likely to experience significant COPD exacerbations. — Mulholland and Greenfield's

(c) Metaplastic and Neoplastic Complications

• Barrett Esophagus: Replacement of normal squamous epithelium with specialized intestinal metaplasia (columnar epithelium with goblet cells) in response to chronic reflux. Associated with more severe, longer-duration GERD, often beginning at a younger age. Affects approximately 11% of patients with GERD.
  • Risk of progression: Barrett esophagus → low-grade dysplasia → high-grade dysplasia → esophageal adenocarcinoma.
  • Surveillance endoscopy recommended at intervals based on presence/grade of dysplasia.
• Esophageal adenocarcinoma: Occurs in ~1% of GERD patients (higher in those with Barrett); arises at the gastroesophageal junction. — Cummings Otolaryngology; Clinical GI Endoscopy

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4. Achalasia of the Cardia

Definition and Pathophysiology

Chicago Classification (HRM Subtypes)

Clinical Features

• Progressive dysphagia to both solids and liquids (key differentiator from mechanical obstruction)
• Regurgitation of undigested food
• Chest pain, weight loss
• Nighttime aspiration, cough

Diagnosis

• Barium swallow: Classic "bird-beak" tapering at LES; dilated, fluid-filled esophagus
• HRM (manometry): Diagnostic — impaired LES relaxation (elevated integrated relaxation pressure) + absent peristalsis; subtyping
• Endoscopy: Exclude pseudoachalasia (malignancy at EGJ); characteristic "pop" on entering stomach

Treatment

1. Pharmacologic (temporizing only):
   • Sublingual nitrates (isosorbide dinitrate) or calcium channel blockers (nifedipine) before meals
   • Side effects limit long-term use
   • Botulinum toxin injection into LES: effective ~65–85%, but effects wane within 6–12 months; reserved for poor surgical candidates
2. Pneumatic dilation:
   • Forceful balloon dilation disrupts LES circular muscle fibers
   • ~90% efficacy; preferred initial therapy for Type II achalasia (100% efficacy in European RCT)
   • Risk of perforation ~1%
3. Laparoscopic Heller Myotomy (LHM):
   • Division of LES circular muscle fibers; combined with partial fundoplication to prevent post-op GERD
   • ~90% efficacy; preferred for Type III achalasia
   • European multicenter RCT showed no significant difference vs. pneumatic dilation overall
4. Per-Oral Endoscopic Myotomy (POEM):
   • Endoscopic submucosal tunneling + myotomy
   • Emerging as preferred for Type III due to ability to extend myotomy into esophageal body

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5. Esophageal Diverticula

Classification by Location

(a) Zenker Diverticulum (Pharyngoesophageal / Hypopharyngeal)

• Technically a hypopharyngeal diverticulum, proximal to the UES
• Forms through Killian triangle — an area of weakness between the cricopharyngeal sphincter and the inferior pharyngeal constrictor
• Primary defect: incomplete relaxation of the UES → increased intraluminal pressure → herniation
• Symptoms: oropharyngeal dysphagia, regurgitation of undigested food, halitosis, aspiration pneumonia
• Diagnosis: barium swallow
• Treatment: symptomatic cases — open surgical resection + cricopharyngeal myotomy; or endoscopic stapling/laser division of the septum (Dohlman procedure)

(b) Mid-Esophageal Diverticula

• Most are asymptomatic
• Traction type (true diverticula): external pull from adjacent inflammation (e.g., tuberculous mediastinal lymphadenitis) — the only true diverticula of the esophagus
• Pulsion type: result from elevated intraluminal pressure, associated with motility disorders

(c) Epiphrenic Diverticula

• Located in the distal esophagus, near the diaphragmatic hiatus / LES
• Usually result from a motility disorder (achalasia, diffuse esophageal spasm)
• Manometry is mandatory before treatment to identify and address the underlying motor disorder
• Treatment: manage the motility disorder; for symptomatic diverticula — diverticulectomy ± myotomy

(d) Intramural Pseudodiverticulosis

• Multiple small outpouchings on barium swallow or endoscopy
• Not true diverticula — represent dilated submucosal glands
• Associated with acid reflux, esophageal strictures, esophageal cancer

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6. Chemical and Thermal Burns; Scar Strictures of the Esophagus

Chemical Burns (Caustic Esophagitis)

• Mucosal injury occurs within minutes of ingestion
• Alkalis (lye — drain cleaners, household cleaners): Cause liquefaction necrosis — deeper penetration, higher risk of perforation and stricture
• Acids: Cause coagulation necrosis — self-limiting penetration (eschar forms), but associated with gastric rupture
• Progression over weeks to months: wall weakens in first 3 weeks (mucosal sloughing + bacterial invasion), then scar retraction and stricture formation over subsequent months

• Supportive care; IV fluids, NPO, analgesia
• Intubation if epiglottis/larynx involved
• Monitor for perforation (free air on imaging)
• Corticosteroids: controversial for preventing stricture formation
• No induced vomiting (re-exposure of mucosa to caustic)
• Late management: endoscopic dilation of strictures (repeated sessions); surveillance endoscopy for squamous cell carcinoma (long-term risk — ~1000× increased risk)

Thermal Burns

• Rare; hot liquids, steam
• Superficial injury usually; rarely progress to stricture
• Managed conservatively

Scar Strictures

• Sequelae of caustic burns, severe GERD (peptic stricture), radiation therapy, or surgical anastomosis
• Diagnosis: Barium swallow (level, length, morphology), endoscopy with biopsy to exclude malignancy
• Treatment: Endoscopic dilation (bougie / balloon dilators); for refractory cases — temporary stenting, surgical resection and reconstruction

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7. Foreign Bodies in the Esophagus

Anatomic Predisposition

• 70% — Upper esophageal sphincter (UES) — most common
• 20% — Level of aortic arch
• 10% — Lower esophageal sphincter (LES) Also at pathologic narrowings: scar from prior burn, peptic stricture, anastomotic strictures. — K.J. Lee's Essential Otolaryngology

Common Objects

• Coins (most common in children)
• Food bolus/meat impaction (most common in adults, often at Schatzki ring or stricture)
• Button batteries — most dangerous due to leakage of alkaline contents and generation of electrical current causing rapid, severe tissue necrosis
• Bones (fish, chicken)
• Dentures, toys

Diagnosis

• Plain radiograph (AP + lateral): First step — identifies radio-opaque objects (coins, batteries), free air (perforation). A coin in the esophagus lies in the coronal plane (face-on on AP), while in the trachea it lies in the sagittal plane (edge-on).
• CT scan: Better characterization of location, type, and complications
• Esophagram: Confirms food disimpaction; no role in initial workup for solid foreign bodies

Management

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Summary Table

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• Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th ed.
• Mulholland and Greenfield's Surgery: Scientific Principles and Practice, 7th ed.
• Cummings Otolaryngology Head and Neck Surgery, 7th ed.
• K.J. Lee's Essential Otolaryngology, 11th ed.
• Rosen's Emergency Medicine: Concepts and Clinical Practice, 10th ed.
• Goldman-Cecil Medicine, International Edition