ESOPHAGUS

Diseases of the esophagus:

Anatomic and motor disorders
Esophageal varices
Esophagitis
Barrett esophagus
Esophageal tumors

ESOPHAGUS
Symptoms:

Dysphagia (difficulty in swallowing)

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

Esophageal mucosal webs

Uncommon
protrusions
of
the
mucosa & submucosa
into the esophageal
lumen.

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

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

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

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

ANATOMIC AND MOTOR DISORDERS

Achalasia
Hiatal hernia
Diverticula

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.
Aperistalsis

Etiology

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

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

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).

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

Achalasia

Birds 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)

I. The axial (sliding) hernia

95% of cases
Protrusion of the
stomach above the
diaphragm
producing a bellshaped dilation.

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
Complications:
Reflux esophagitis
Mucosal ulceration
Bleeding
Perforation

II. The non-axial (paraesophageal)

hernia
A separate portion
of the stomach,
usually along the
greater curvature,
enters the thorax
through
the
widened foramen .

Clinical picture
Rarely induce reflux
Complications:
May
become
strangulated
or
obstructed.
Less common: Ulceration, bleeding,
perforation.

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.
Traction diverticulum near the midpoint of
the esophagus.
Epiphrenic
diverticulum
above the LES.

immediately

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

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

Diverticula

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).
Most often the consequence of portal
hypertension, commonly due to cirrhosis
(hepatitis, alcohol, shistosomiasis ).

Clinical picture and

treatment
Asymptomatic

If ruptured Massive hematemesis.

It subsides spontaneously in 50% of cases.
20 - 30% die during the 1st episode.
Rebleeding in a 70% within 1 year, with a similar rate of
mortality for each episode.

Treatment:
Sclerotherapy,
endoscopic
thrombotic agents.
Balloon tamponade.
Ligation.

injection

of

Esophageal varices

Esophageal varices

Dilated varice beneath intact squamous mucosa.

ESOPHAGITIS
Inflammation of the esophageal mucosa

A common condition worldwide.

High prevalence in northern Iran & china

Causes:
Reflux esophagitis (GERD): Most common
Chemical esophagitis: Ingestion of irritants
(alcohol, corrosives, excessively hot fluids, heavy
smoking, pill-induced, anticancer CTX & RTX ).
Infectious esophagitis: HSV, CMV, candidiasis
Others: Uremia, Crohn disease, skin disease,
GVHD.

Reflux esophagitis (GERD)

Reflux of gastric contents into lower esophagus
is the most important cause of esophagitis.
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

Contributory factors of GERD

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

is

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

Severe reflux esophagitis

Marked hypremia with focal hemorrhage

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

Reflux esophagitis

Basal zone hyperplasia & elongation of LP papillae

Reflux esophagitis

Intraepithelial inflammatory cells including eosinophils

Complications

Bleeding
Ulceration
Development of stricture
Barrett esophagus, with increased
risk of adenocarcinoma

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

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).
Origin of columnar cells:
Migration of gastric mucosa OR
More commonly from growth & differentiation
of stem cells.

Gross appearance
Salmon-pink, velvety mucosa
Located between the smooth pale-pink
squamous mucosa and the light brown gastric
mucosa.

May exist as:

Tongues" extending up from the GEJ, or
An irregular circumferential band, or
Isolated patches (islands) in distal esophagus.

Long segment (> 2cm) or short segment

(<2cm)*.

Normal esophagus

Barrett esophagus

Barrett esophagus - endoscopy

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.
It is important to look for the presence &
the grade of dysplasis (low grade or high
grade).

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

Barrett esophagus

Esophageal tumors
Benign tumors
Leiomyoma (most common).
Squamous papilloma.

Malignant tumors:
Esophageal carcinoma:
Squamous cell carcinoma
Adenocarcinoma

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

Squamous cell carcinoma

The most common type of esophageal
carcinoma.
Age: adults > 45 years
Gender: Male > female
Geographic:
High incidence in Iran, China & South Africa

Race: More in black.

Dysplasia CIS invasive carcinoma

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, C, riboflavin, thiamine,
pyridoxine)
Deficiency of trace metals (zinc)
Fungal contamination of foodstuffs
High content of nitrites/nitrosamines
Human papilloma virus
Genetic Predisposition ??

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

Exophytic , infiltrative and ulcerated SCC

Squamous cell carcinoma

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

precursor

of

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

Clinical Features of esophageal CA

Early asymptomatic
Progressive dysphagia and odynophagia
due to obstruction.
Weight loss, anorexia, fatigue, and
weakness.
Diagnosis is usually made by imaging
techniques and endoscopic biopsy.

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