Diseases of the esophagus:
• Anatomic and motor disorders
• Esophageal varices
• Esophagitis
• Barrett esophagus
• Esophageal tumors


Dysphagia (difficulty in swallowing)
Odynophagia (painful swallowing)
Heartburn (retrosternal burning pain)
Hematemesis (vomiting of blood)
Melena (blood in the stools)

Esophageal mucosal webs
• Uncommon
mucosa & submucosa
into the esophageal

• Semi-circumferential
& eccentric
• Most common in the
upper esophagus.

Esophageal mucosal webs Etiology: • Congenital • Acquired  long-standing reflux esophagitis  Chronic graft-versushost disease  Blistering skin diseases Paterson-Brown-Kelly (Plummer-Vinson) syndrome: Upper esophageal web Iron-deficiency anemia Atrophic glossitis • ⇑ risk of postcricoid esophageal carcinoma .

• The rings consist of mucosa. . and sometimes a hypertrophied muscularis propria.Esophageal rings • Concentric plates of tissue protruding into the lumen of distal esophagus. submucosa.

Esophageal stenosis Causes: • Occasionally congenital • More commonly acquired as a result of severe esophageal injury and inflammatory scarring:  Gastroesophageal reflux  Scleroderma  Radiation  Caustic injury. .

Clinical picture: • Stenosis usually develops in adulthood • Progressive dysphagia to solid then to fluid . particularly the submucosa. • The lining epithelium is thin ± ulcerated.Esophageal stenosis Microscopic picture: • Fibrous thickening of the esophageal wall. • Atrophy of the muscularis propria.

ANATOMIC AND MOTOR DISORDERS • Achalasia • Hiatal hernia • Diverticula .

• Aperistalsis .Achalasia (failure to relax) Definition: “Incomplete relaxation of the LES in response to swallowing”. Three major abnormalities: • Incomplete relaxation of the LES with swallowing • Increased resting tone of the LES.

Etiology • Primary achalasia: Loss of intrinsic inhibitory innervation of the LES and smooth muscle. Idiopathic: ?? Autoimmunity. previous viral infection… * .

and ureter.Etiology • Secondary achalasia Chagas disease (Trypanosoma cruzi)  Causes destruction of the myenteric plexus of the esophagus duodenum. colon. Disorders of the dorsal motor nuclei:  Poliomyelitis & autonomic neuropathy in DM Infiltrative disorders:  Malignancy. sarcoidosis . amyloidosis.

Pathophysiology • Functional obstruction of the esophagus • Progressive dilation of the esophagus above the level of the LES • The wall of the esophagus may be: Of normal thickness. Thick (Hypertrophy of the muscularis). . Thinned (by dilation).

but may appear in infancy or childhood.Clinical picture • Age: usually in young adults. • Dysphagia to solid and fluid • Nocturnal regurgitation Complications: • Aspiration of undigested food • Esophageal squamous cell carcinoma in 5% .

Achalasia Bird’s beak or rat tail appearance .

Hiatal Hernia • Hiatal hernias present in 1% to 20% of adults • Characterized by:  Separation of the diaphragmatic crura  Widening of the space between the muscular crura and the esophageal wall  Dilated segment of the stomach protrude above the diaphragm. • Two anatomic patterns • Axial (sliding) & non-axial (paraesophageal) .

The axial (sliding) hernia • 95% of cases • Protrusion of the stomach above the diaphragm producing a bellshaped dilation.I. .

Clinical picture
• 10% suffer from symptoms:
Heartburn or regurgitation of gastric juices
into the mouth due to incompetent LES.
Symptoms are accentuated by bending
forward, lying supine, and obesity …
Reflux esophagitis
Mucosal ulceration

II. The non-axial (paraesophageal)
• A separate portion
of the stomach,
usually along the
greater curvature,
enters the thorax
widened foramen .

Clinical picture
• Rarely induce reflux
• May
• Less common: Ulceration, bleeding,

Diverticula • True diverticulum: An outpouching of the alimentary tract that contains all visceral layers. . • False diverticulum: An outpouching of mucosa and submucosa only.

Esophageal diverticula • Diverticula of esophagus may develop in three regions:  Zenker diverticulum (pharyngoesophageal diverticulum) immediately above the UES. immediately .  Epiphrenic diverticulum above the LES.  Traction diverticulum near the midpoint of the esophagus.

Zenker diverticulum • Etiology: Disordered cricopharyngeal motor function ± GERD • Clinical picture: May reach several cms and accumulate food. Dysphagia & food regurgitation Mass in the neck Aspiration pneumonia is a significant risk .

Zenker diverticulum .

Asymptomatic • Epiphrenic diverticula Dyscoordination of peristalsis & LES relaxation May lead to nocturnal regurgitation of massive amounts of fluid .Diverticula • Traction diverticula Due to wall weakening as seen in TB of mediastinal LNs. motor dysfunction or congenital.

Diverticula .

. commonly due to cirrhosis (hepatitis. alcohol. • Most often the consequence of portal hypertension.ESOPHAGEAL VARICES • Dilated tortuous veins in the mucosa & submucoa of the lower 1/3 of esophagus & proximal stomach (at site of communication between portal and systemic circulation). shistosomiasis …).

30% die during the 1st episode.  It subsides spontaneously in 50% of cases. • Balloon tamponade.  Rebleeding in a 70% within 1 year. with a similar rate of mortality for each episode.  20 . injection of . endoscopic thrombotic agents. Treatment: • Sclerotherapy. • Ligation.• Clinical picture and treatment Asymptomatic • If ruptured  Massive hematemesis.

Esophageal varices .

.Esophageal varices Dilated varice beneath intact squamous mucosa.

candidiasis … Others: Uremia. GVHD. • High prevalence in northern Iran & china • • • • Causes: Reflux esophagitis (GERD): Most common Chemical esophagitis: Ingestion of irritants (alcohol. excessively hot fluids. Crohn disease. . Infectious esophagitis: HSV. pill-induced. skin disease. heavy smoking. CMV.ESOPHAGITIS “Inflammation of the esophageal mucosa” • A common condition worldwide. anticancer CTX & RTX …). corrosives.

Clinical picture of GERD: • Age: usually adults > 40 y Occasionally seen in infants & children • Recurrent heartburn (dominant symptom). • Dysphagia • Regurgitation + sour tasting • Rarely. chest pain .Reflux esophagitis (GERD) • Reflux of gastric contents into lower esophagus is the most important cause of esophagitis.

no obvious etiology identifiable Sliding hiatal hernia Inadequate clearance of refluxed material Delayed gastric emptying Increased gastric volume is .Contributory factors of GERD Decreased efficacy of antireflux mechanisms: CNS depressants Alcohol or tobacco exposure Prolonged gastric intubation In most cases.

Gross appearance • The anatomic changes depend on: The causative agent. • Mild esophagitis: Simple hyperemia • Severe esophagitis: Epithelial erosions or ulceration into the submucosa. The duration & severity of the exposure. .

Severe reflux esophagitis Marked hypremia with focal hemorrhage .

Intraepithelial neutrophils are markers of severity. Elongation of lamina propria papillae with congested capillaries. Basal zone hyperplasia (N 10-15% of epithelial thickness). •. Eosinophils with or without neutrophils. 3. severity of symptoms is not closely related to the degree of histologic picture. in the epithelial layer . .Microscopic appearance • Three characteristic histologic features: 1. •. 2.

Reflux esophagitis Basal zone hyperplasia & elongation of LP papillae .

Reflux esophagitis Intraepithelial inflammatory cells including eosinophils .

with increased risk of adenocarcinoma .Complications • • • • Bleeding Ulceration Development of stricture Barrett esophagus.

• Gender: M: F is 4:1 • Race: common in white. . • Occurs in ~ 10% of patients with longstanding reflux.BARRETT ESOPHAGUS • Definition: “The replacement of the distal esophageal squamous mucosa by metaplastic columnar epithelium above the level of LES”.

Origin of columnar cells: • Migration of gastric mucosa OR • More commonly from growth & differentiation of stem cells.Pathogenesis • Prolonged and recurrent reflux • Inflammation and ulceration of the squamous epithelium • Healing and re-epithelization lead to columnar mucosa (more resistant to gastric acid). .

velvety mucosa  Located between the smooth pale-pink squamous mucosa and the light brown gastric mucosa. or  Isolated patches (islands) in distal esophagus. • May exist as:  “Tongues" extending up from the GEJ. • Long segment (> 2cm) or short segment (<2cm)*. .Gross appearance • Salmon-pink. or  An irregular circumferential band.

Normal esophagus Barrett esophagus .

Barrett esophagus .endoscopy .

• It is important to look for the presence & the grade of dysplasis (low grade or high grade).Microscopic appearance • The squamous epithelium is replaced by metaplastic columnar epithelium (gastric or intestinal containing goblet cells). • Barrett mucosa may be focal and require repeated endoscopy and biopsy. .

The risk is higher in high grade dysplasia Periodic screening for high-grade dysplasia with esophageal biopsy is recommended .Complications • Ulcer “Barrett ulcer” • Stricture • Dysplasia & ↑ risk of adenocarcinoma Affects 1% of Barrette per year (30-100 fold over the general population).

Barrett esophagus .

Esophageal tumors • Benign tumors Leiomyoma (most common). Squamous papilloma. • Malignant tumors: Esophageal carcinoma: • Squamous cell carcinoma • Adenocarcinoma .

.  In the US & west. adenocarcinoma arising in Barrett esophagus has increased (~ 50%).Esophageal carcinoma • Incidence:  Worldwide. squamous cell carcinomas constitute 90% of esophageal cancers.

• Age: adults > 45 years • Gender: Male > female • Geographic:  High incidence in Iran.Squamous cell carcinoma • The most common type of esophageal carcinoma. China & South Africa • Race: More in black. Dysplasia  CIS  invasive carcinoma .

pyridoxine) Deficiency of trace metals (zinc) Fungal contamination of foodstuffs High content of nitrites/nitrosamines Human papilloma virus Genetic Predisposition ?? . riboflavin. thiamine. C.Risk Factors for SCC of the Esophagus Esophageal Disorders: Long-standing esophagitis Achalasia Plummer-Vinson syndrome Caustic injury Life-style (most important): Alcohol consumption Tobacco abuse Dietary: Deficiency of vitamins (A.

50% in the middle 1/3. Diffuse & infiltrative causing thickening of the wall & narrowing of the lumen.Gross appearance • There are 3 morphologic patterns: 1. & 30% in the lower 1/3. Site: 20% arise in the upper 1/3. •. . Polypoid exophytic masses. most common 2. Ulcerated & necrotic 3.

Exophytic . infiltrative and ulcerated SCC .

Squamous cell carcinoma .

• No association with alcohol. Tobacco. Obesity . precursor of .Adenocarcinoma • Risk factors: Barrett esophagus is the esophageal adenocarcinoma. Radiation. • Race: more common in white.

The development of adenocarcinomas from Barrett esophagus is a multistep process The degree of dysplasia is the strongest predictor of the progression to cancer .

Gross appearance • Site: Usually in the distal 1/3 • May invade the subjacent gastric cardia • Initially appear as flat or raised patches • May develop into large nodular masses or ulcerative or diffuse infiltrative patterns. .

Adenocarcinoma arising in a background of Barrett esophagus .

Microscopic picture • Adenocarcinoma • Mucin-producing glandular tumors showing intestinal-type features .

• Diagnosis is usually made by imaging techniques and endoscopic biopsy. • Weight loss.Clinical Features of esophageal CA • Early asymptomatic • Progressive dysphagia and odynophagia due to obstruction. and weakness. fatigue. . anorexia.

Prognosis of esophageal CA • Prognosis is generally poor • Symptomatic tumors are generally very large at diagnosis and have already invaded the esophageal wall. • Stage is the most important prognostic factor • Surgical excision is rarely curative. . submucosal lymphatics and adjacent structures early.