DISORDERS OF

ESOPHAGUS
BY KANG’OMBE C KAKENGE
 ESOPHAGUS
Normal Anatomy
- The oesophagus is a muscular tube
extending from the pharynx to the
stomach.
- 25(10 Inches) cm in length in adults
From the incisors to lower
oesophageal sphincter at 40 cm
The region of proximal oesophagus at the
level of cricopharyngeal muscle is called the
upper oesophagus sphincter, while the
portion adjacent to the anatomic
gastroesophageal junction is referred to as
lower oesophageal sphincter (Cardiac
sphincter).
 •HISTOLOGY
 Lined by stratified squamous non-
keratinized epithelium

The wall of the esophagus consists o f mucosa

muscularis propria and adventitia/serosa
 FUNCTION CORRELATION: Esophagus

The major function of the esophagus is to convey liquids or a mass of chewed food (bolus)
from the oral cavity to the stomach. For this function, the lumen of the esophagus is lined by
a protective nonkeratinized stratified squamous epithelium. Aiding in this function are
esophageal glands located in the connective tissue of the wall. There are two types of
glands in the wall of the esophagus. The esophageal cardiac glands are present in the lamina
propria of the upper and lower regions of the esophagus. These glands have a similar
morphology to those found in the cardia of the stomach, where the esophagus terminates.
Esophageal glands proper are located in the connective tissue of the submucosa. Both types
of glands produce the secretory product mucus, which is conducted in excretory ducts
through the epithelium to lubricate the esophageal lumen. The swallowed material is
moved from one end of the esophagus to the other by strong muscular contractions called
peristalsis. At the lower end of the esophagus, a muscular gastroesophageal sphincter
constricts the lumen and prevents regur-gitation of swallowed material into the of
swallowed material into the esophagus .
 ATRESIA

Atresia is absence of opening (lumen)/non-canalization.

Atresia, in which a thin, noncanalized cord replaces a segment of
oesophagus, is more common. Atresia occurs most commonly at or
near the tracheal bifurcation and usually is associated with a fistula
connecting the upper or lower oesophageal pouches to a bronchus
or the trachea. This abnormal connection can result in aspiration,
suffocation, pneumonia, or severe fluid and electrolyte imbalances.

Fistula: An abnormal passage leading from a suppurating cavity to the body surface .
 Stenosis
Abnormal narrowing of the oesophageal lumen is called
oesophageal stenosis. Passage of food can be impeded by
oesophageal stenosis.
The narrowing generally is caused by fibrous thickening of the
submucosa, atrophy of the muscularis propria, and secondary
epithelial damage. Stenosis most often is due to inflammation and
scarring, which may be caused by chronic gastroesophageal reflux,
irradiation, or caustic (acid) injury.
Stenosis associated dysphagia usually is progressive; difficulty
eating solids typically occurs long before problems with liquids.
ACHALASIA/ CARDIOSPASM (MEGA ESOPHAGUS)
Achalasia is a disorder of motility (neuromuscular disorder) Of
oesophagus, characterized by incomplete relaxation of the
LES (Cardiac sphincter) in response to swallowing with dilation
of the proximal oesophagus.
Increased tone of the lower oesophageal sphincter(LES), as a
result of impaired smooth muscle relaxation, is an important
cause of oesophageal obstruction. Achalasia is characterized
by the triad of incomplete LES relaxation, increased LES tone,
and aperistalsis of the oesophagus.
 ACHALASIA AETIOLOGY

There is loss of intramural neurons in the wall of the oesophagus.

Most cases are of primary idiopathic achalasia which may be congenital.
Secondary achalasia may occur from some other causes which includes:
Chagas' disease (an epidemic parasitosis with Trypansoma cruzi), infiltration
into esophagus by gastric carcinoma or lymphoma, certain viral infections, and
neurodegenerative diseases.
 MORPHOLOGY

• There is dilatation above the short contracted terminal segment of the

oesophagus.
• Muscularis propria of the wall may be of normal thickness, hypertrophied as
a result of obstruction, or thinned out due to dilatation. Secondary
oesophagitis may supervene and cause oesophageal ulceration and
haematemesis.
 Hiatal hernia

• Hiatus hernia is the herniation or protrusion of part of the stomach through

the oesophageal hiatus (opening) of the diaphragm.
• Oesophageal hiatal hernia is the cause of diaphragmatic hernia in 98% of
cases.·
• Congenital hiatal hernias are recognized in infants and children,but many
are acquired in later life. Hiatal hernia is symptomatic in fewer than 10% of
adults, and these cases are generally associated with other causes of LES
incompetence. Symptoms, including heartburn and regurgitation of gastric
juices, are similar to GERD.
 Hiatal hernia causes
• The basic defect is the failure of the muscle fibres of the diaphragm that form the margin of
the oesophageal hiatus. This occurs due to shortening of the oesophagus which may be
congenital or acquired. Congenitally short oesophagus may be the cause of hiatus hernia in
a small proportion of cases.
• More commonly, it is acquired due to secondary factors which cause fibrous scarring of the
oesophagus as follows:
a) Degeneration of muscle due to aging.
b) Increased intra-abdominal pressure such as in pregnancy, abdominal tumours etc.
c) Recurrent oesophageal regurgitation and spasm causing inflammation and fibrosis.
d) Increase in fatty tissue in obese people causing decreased muscular elasticity of
diaphragm.
 Morphology
• There are 3 patterns in hiatus hernia :
i) Sliding or oesophagi-gastric hernia is the most common, occurring in 85%
of cases. The herniated part of the stomach appears as supradiaphragmatic
bell due to sliding up on both sides of the oesophagus.
ii) Rolling or para-oesophageal hernia is seen in 10% of cases. This is a true
hernia in which cardiac end of the stomach rolls up para-oesophageally,
producing an intrathoracic sac.
iii) Mixed or transitional hernia constitutes the remaining 5% cases in which
there is combination of sliding and rolling hiatus hernia.
 Esophageal varices

• Oesophageal varices are tortuous, dilated and engorged

oesophageal veins, seen along the longitudinal axis of
oesophagus. They occur as are suit of elevated pressure in the
portal venous system, most commonly in cirrhosis of the liver .
Less common causes are: portal vein thrombosis, hepatic vein
thrombosis . The lesions occur as a result of bypassing of portal
venous blood from the liver to the oesophageal venous plexus.
The increased venous pressure in the superficial veins of the
oesophagus may result in ulceration and massive bleeding.
 Esophageal varices
• Instead of returning directly to the heart, venous blood from the
gastrointestinal tract is delivered to the liver via the portal vein before
reaching the inferior vena cava. 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, which
can lead to the development of oesophageal varices, an important cause of
oesophageal bleeding.

Varix; An abnormally enlarged and twisted blood vessel.

 Pathogenesis
One of the few sites where the splanchnic (visceral) and systemic
venous circulations can communicate is the oesophagus. Thus, portal
hypertension induces development of collateral channels that allow portal blood
to shunt (divert) into the system. However, these collateral veins enlarge the
subepithelial and submucosal venous Plexi within the distal oesophagus. These
vessels, termed varices, develop in 90% of cirrhotic patients, most commonly in
association with alcoholic liver disease.

Worldwide, hepatic schistosomiasis is the second most common cause of varices.

 Morphology

• Varices can be detected by angiography and appear as

tortuous dilated veins lying primarily within the submucosa
of the distal oesophagus and proximal stomach. Varices
may not be obvious on gross inspection of surgical or
postmortem specimens, because they collapse in the
absence of blood flow. The overlying mucosa can be intact
but is ulcerated and necrotic if rupture has occurred.
 Clinical features
Varices often are asymptomatic, but their rupture can lead to massive
Hematemesis and death. Variceal rupture therefore constitutes a medical
emergency. Despite intervention, as many as half of the patients die from the
first bleeding episode, either as a direct consequence of haemorrhage or due
to hepatic coma triggered by the protein load that results from intraluminal
bleeding and hypovolemic shock. Among those who survive, additional
episodes of haemorrhage, each potentially fatal, occur in more than 50% of
cases. As a result, greater than half of the deaths associated with advanced
cirrhosis result from cancel rupture .
 Esophagitis
Inflammation of esophagus ( after injury to esophageal mucosa)
Predisposing factors/origins/ causes:
 Prolonged gastric intubation,
 Ingestion of corrosive or irritant substances
 Radiation
 Chemotherapy
 Laceration: Malloy Weiss tears
Longitudinal and superficial tears in the oesophagus near the
gastroesophageal junction are termed Mallory-Weiss tears, and are most
often associated with severe retching (strain to vomit) Or vomiting secondary
to acute alcohol intoxication. Normally, a reflex relaxation of the
gastroesophageal musculature precedes the ant peristaltic contractile wave
associated with vomiting. This relaxation is thought to fail during prolonged
vomiting, with the result that refluxing gastric contents overwhelm the gastric
inlet and cause the oesophageal wall to stretch and tear. Patients often
present with hematemesis.
 Types /causes of esophagitis

Reflux esophagitis-GERD
CHEMICAL AND INFECTIOUS ESOPHAGITIS
EOSINOPHILIC ESOPHAGITIS
Barrett Esophagus
Herpes simplex esophagitis
Cytomegalovirus (CMV) esophagitis
Candida esophagitis
Crohn's diseaseIdiopathic eosinophilic esophagitis
Other types of esophagitis include those caused by tuberculosis, blastomycosis, drugs,
allergic reactions, irradiation and ingestion of corrosive chemicals.
 Reflux Esophagitis GERD

• The stratified squamous epithelium of the

oesophagus is resistant to abrasion from foods but is sensitive to ACID.
Submucosal glands, which are most abundant in the proximal and distal
oesophagus, contribute to mucosal protection by secreting MUCIN and
BICARBONATE.
 Reflux Esophagitis GERD

• Constant LES tone prevents reflux of acidic gastric contents, which are
under positive pressure and would otherwise enter the oesophagus.
• Reflux of gastric contents into the lower oesophagus(due to decreased LES
tone) is the most frequent cause of esophagitis. The associated clinical
condition is termed gastroesophageal reflux disease (GERD).
 Pathogenesis

• Conditions that decrease lower esophageal sphincter tone or increase abdominal pressure contribute to GERD and
include:
Alcohol
Tobacco use,
Obesity,
Central nervous system depressants,
Pregnancy,
Hiatal hernia,
Delayed gastric emptying, and
Increased gastric volume.
In many cases, no definitive cause is identified
.
 Clinical features

• GERD is most common in adults over age 40 but also occurs in infants and
children. The most common clinical symptoms are dysphagia, heartburn,
and, less frequently, noticeable regurgitation of sour-tasting gastric
contents.
• Rarely, chronic GERD is punctuated by attacks of severe chest pain that may
be mistaken for heart disease.
 Treatment

Treatment with proton pump inhibitors or H,

histamine receptor antagonists, which reduce gastric acidity, typically
provides symptomatic relief.
 complications

ESOPHAGEAL ULCERATION,
HEMATEMESIS,
MELENA’
STRICTURE DEVELOPMENT