Congenital Anomalies, Inflammatory

& Neoplastic Disorders of Esophagus

Dr Muhammad Omair Riaz

Esophagus - Pathology

Congenital anomalies

Inflammatory disorders

Neoplastic disorders

Esophagus – Congenital Anomalies

Tracheoesophageal fistula

Esophageal atresia

Esophagus – Congenital Anomalies

Effects

Either form of fistula can lead to aspiration,

suffocation, pneumonia, and severe fluid and

electrolyte imbalances.

Developmental abnormalities of the esophagus are

associated with congenital heart defects,

genitourinary malformations, and neurologic disease.

Esophagus – Inflammatory disorders

Lacerations

Chemical and Infectious Esophagitis

Reflux Esophagitis

Eosinophilic Esophagitis

Esophageal Varices

Barrett Esophagus

Lacerations

Longitudinal mucosal tears near the

gastroesophageal junction are termed Mallory-

Weiss tears

Most often associated with severe retching or

vomiting secondary to acute alcohol intoxication.

Lacerations

Mechanism

Normally, a reflex relaxation of the gastroesophageal

musculature precedes the antiperistaltic contractile

wave associated with vomiting. It is speculated that

this relaxation fails during prolonged vomiting, with

the result that refluxing gastric contents overwhelm

the gastric inlet and cause the esophageal wall to

stretch and tear.

These tears usually cross the gastroesophageal

junction and may also be located in the proximal

gastric mucosa.

Chemical and Infectious Esophagitis

Stratified squamous mucosa of the esophagus may

be damaged by a variety of irritants including

alcohol, corrosive acids or alkalis, excessively hot

fluids, and heavy smoking.

Symptoms range from self-limited pain, particularly

on swallowing, that is, odynophagia, to hemorrhage,

stricture, or perforation in severe cases

Chemical and Infectious Esophagitis

Esophageal infections in otherwise healthy

individuals are uncommon

Most often due to herpes simplex virus.

Infections in patients who are debilitated or

immunosuppressed, as a result of disease or

therapy, is more common and can be caused by

herpes simplex virus, cytomegalovirus (CMV), or

fungal organisms. Among fungi, candidiasis is most

common, although mucormycosis and aspergillosis

are also seen.

Reflux Esophagitis

The stratified squamous epithelium of the esophagus

is resistant to abrasion from foods but is sensitive to

acid.

Submucosal glands, which are most abundant in the

proximal and distal esophagus, contribute to

mucosal protection by secreting mucin and

bicarbonate.

The tone of the lower esophageal sphincter prevents

reflux of acidic gastric contents, which are under

positive pressure and would otherwise enter the

esophagus.

Reflux of gastric contents into the lower

esophagus is the most frequent cause of

esophagitis

Esophageal Varices

Venous blood from the GI tract passes through the

liver, via the portal vein, before returning to the heart.

This circulatory pattern is responsible for the first-

pass effect in which drugs and other materials

absorbed in the intestines are processed by the liver

before entering the systemic circulation.

Diseases that impede this flow cause portal

hypertension and can lead to the development of

esophageal varices

Pathogenesis

Portal hypertension results in the development

of collateral channels at sites where the portal

and caval systems communicate.

These collateral veins allow some drainage to occur,

but at the same time they lead to development of

congested subepithelial and submucosal venous

plexi within the distal esophagus and proximal

stomach.

These vessels, termed varices, develop in the vast

majority of cirrhotic patients, most commonly in

association with alcoholic liver disease

Morphology

Varices are tortuous dilated veins lying primarily within

the submucosa of the distal esophagus and proximal

stomach. Venous channels directly beneath the

esophageal epithelium may also become massively

dilated.

Varices may not be grossly obvious in surgical or

postmortem specimens, because they collapse in the

absence of blood flow and are obscured by the overlying

mucosa.

Variceal rupture results in hemorrhage into the lumen or

the esophageal wall, in which case the overlying mucosa

appears ulcerated and necrotic. If rupture has occurred in

the past, venous thrombosis, inflammation, and evidence

of prior therapy may also be present.

Clinical Features

Gastroesophageal varices are present in nearly half

of the patients with cirrhosis, and 25-40% of patients

with cirrhosis develop variceal bleeding.

Approximately 12% of previously asymptomatic

varices bleed each year.

Variceal hemorrhage is an emergency.

Barret Esophagus

A complication of chronic GERD that is

characterized by intestinal metaplasia within the

esophageal squamous mucosa.

The incidence of Barrett esophagus is rising, and it is

estimated to occur in as many as 10% of individuals

with symptomatic GERD.

Barrett esophagus is most common in white males

and typically presents between 40 and 60 years of

age.

The greatest concern in Barrett esophagus is that it

confers an increased risk of esophageal

adenocarcinoma.

Morphology

Diagnosis of Barrett esophagus requires endoscopic

evidence of metaplastic columnar mucosa above the

gastroesophageal junction.

Microscopically, intestinal-type metaplasia is seen as

replacement of the squamous esophageal epithelium

with goblet cells.

These are diagnostic of Barrett esophagus

Esophagus - Neoplastic disorders

Esophageal Tumors

Adenocarcinoma

Squamous Cell Carcinoma

Esophagus - Neoplastic disorders

The vast majority of esophageal cancers fall into one

of two types

Adenocarcinoma

Squamous cell carcinoma.

Esophagus - Adenocarcinoma

Most esophageal adenocarcinomas arise from

Barrett esophagus.

Increased rates of esophageal adenocarcinoma may

be partly due to the increased incidence of obesity-

related gastroesophageal reflux and Barrett

esophagus.

Additional risk factors include tobacco use and

exposure to radiation.

Conversely, risk is reduced by diets rich in fresh

fruits and vegetables. Some serotypes of

Helicobacter pylori are associated with decreased

risk of esophageal

Esophagus – Adenocarcinoma

Morphology

Esophageal adenocarcinoma usually occurs in the

distal third of the esophagus and may invade the

adjacent gastric cardia.

Initially appearing as flat or raised patches in

otherwise intact mucosa, large masses of 5 cm or

more in diameter may develop.

Alternatively, tumors may infiltrate diffusely or

ulcerate and invade deeply. Microscopically, Barrett

esophagus is frequently present adjacent to the

tumor. Tumors most commonly produce mucin and

form glands often with intestinal-type morphology;

Esophagus – Squamous Cell Carcinoma

Esophageal squamous cell carcinoma occurs in adults

older than age 45 and affects males four times more

frequently than females.

Risk factors include alcohol and tobacco use, poverty,

caustic esophageal injury, achalasia, tylosis, Plummer-

Vinson syndrome, diets that are deficient in fruits or

vegetables, and frequent consumption of very hot

beverages.

Previous radiation to the mediastinum also predisposes

individuals to esophageal carcinoma

Esophageal squamous cell carcinoma is nearly eight-fold

more common in African Americans than Caucasians

Esophagus – Squamous Cell Carcinoma

Morphology

Polypoid, or exophytic tumors, protrude into and

obstruct the lumen.

Maybe either ulcerated or diffusely infiltrative lesions

that spread within the esophageal wall and cause

thickening, rigidity, and luminal narrowing.

They may invade surrounding structures including

the respiratory tree, causing pneumonia; the aorta,

causing catastrophic exsanguination; or the

mediastinum and pericardium.

Most squamous cell carcinomas are moderately to

welldifferentiated

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