2. Esophagus
Normal Anatomy
– The esophagus is a muscular tube
extending from the pharynx to
the stomach.
– 25 (10 inches) cm in length in
adults.
From the incisors to lower
esophageal sphincter at 40 cm
The region of proximal oesophagus at
the level of cricopharyngeus muscle is
called the upper oesophageal
sphincter, while the portion adjacent
to the anatomic gastrooesophageal
junction is referred to as lower
oesophageal sphincter (Cardiac
sphincter).
3. Histology
– Lined by stratified
squamous non-keratinized
epithelium.
The wall of the oesophagus consists of
mucosa,
submucosa,
muscularis propria (muscularis externa)
and adventitia/ serosa
(Intraabdominal part).
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9. Obstructive & Vascular diseases
• Mechanical Obstruction: Atresia, Stenosis
• Function Obstruction: Achalasia
• Ectopia/developmental rests: upper third of esophagus
• Esophageal Varices:
10. Atresia
Atresia is absence of opening (lumen)/ noncanalization.
Atresia, in which a thin, noncanalized cord replaces a segment of
esophagus, 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 esophageal 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.
11. Trachea
Bronchi
Esophageal atresia and tracheoesophageal fistula. A, Blind upper and
lower esophageal segments. B, Blind upper segment with fistula
between lower segment and trachea. C, Fistula between patent
esophagus and trachea. Type B is the most common.
12. Stenosis
Abnormal narrowing of the esophageal lumen is called
esophageal stenosis. Passage of food can be impeded by
esophageal 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.
Stenosisassociated dysphagia usually is progressive;
difficulty eating solids typically occurs long before problems
with liquids.
13. ACHALASIA/ Cardiospasm (Mega Esophagus)
Achalasia is a disorder of motility (neuromuscular disorder) of
esophagus, characterized by incomplete relaxation
of the LES (Cardiac sphincter) in response to swallowing
with dilation of the proximal esophagus.
Increased tone of the lower esophageal sphincter
(LES), as a result of impaired smooth muscle
relaxation, is an important cause of esophageal
obstruction. Achalasia is characterized by the triad
of incomplete LES relaxation, increased LES tone,
and aperistalsis of the esophagus.
14. AETIOLOGY
Achalasia
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 oesophagus by gastric carcinoma or lymphoma,
certain viral infections, and neurodegenerative diseases.
15. 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.
16. Ectopia/ developmental rests/ Inlet patch
The most frequent site of ectopic gastric mucosa is the upper third of
the esophagus, where it is referred to as an inlet patch. Although
the presence of such tissue generally is asymptomatic, acid released
by gastric mucosa within the esophagus can result in dysphagia,
esophagitis, Barrett esophagus, or, rarely, adenocarcinoma.
17. 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.
18. Causes
Hiatal Hernia
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.
19. Morphology
There are 3 patterns in hiatus hernia :
i) Sliding or oesophago-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.
20.
21. Esophageal Varices
Oesophageal varices are tortuous, dilated and engorged oesophageal
veins, seen along the longitudinal axis of oesophagus. They occur as a
result 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 (Budd-Chiari syndrome)
and pylephlebitis. 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.
22. 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
esophageal varices, an important cause of esophageal bleeding.
Varix: An abnormally enlarged & twisted blood vessel.
23. Pathogenesis
One of the few sites where the splanchnic (visceral) and systemic
venous circulations can communicate is the esophagus. Thus,
portal hypertension induces development of collateral channels
that allow portal blood to shunt (divert) into the caval system.
However, these collateral veins enlarge the subepithelial and
submucosal venous plexi within the distal esophagus. 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.
24. Morphology
Varices can be detected by angiography and appear
as tortuous dilated veins lying primarily within the
submucosa of the distal esophagus 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.
25. 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 hemorrhage 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 hemorrhage, 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 variceal rupture.
26. Esophagitis
Inflammation of esophagus (after injury to esophageal mucosa).
Predisposing factors/Origins/Causes:
• Prolonged gastric intubation,
• Ureamia
• Ingestion of corrosive or Irritant substances
• Radiation
• Chemotherapy
27. Lecerations: Mallory Weiss tears
Longitudinal and superficial tears in the esophagus
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 antiperistaltic
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
esophageal wall to stretch and tear. Patients often present with hematemesis.
Boerhaave syndrome, characterized by transmural esophageal tears and
mediastinitis, occurs rarely and is a catastrophic event.
28. 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 disease
• Idiopathic eosinophilic esophagitis
• Other types of esophagitis include those caused by tuberculosis,
blastomycosis, drugs, allergic reactions, irradiation and ingestion of
corrosive chemicals.
29. Reflux Esophagitis GERD
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.
30. Reflux Esophagitis GERD
Constant LES tone 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
(due to decreased LES tone) is the most frequent cause of
esophagitis .The associated clinical condition is
termed gastroesophageal reflux disease (GERD).
31. Pathogenesis
• Reflux of gastric juices (ACID) is central to the
development of mucosal injury in GERD.
• In severe cases, reflux of BILE from the
duodenum may exacerbate the damage.
32. 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.
33. Morphology
Endoscopy Microscopy
GROSS:
• Simple hyperemia, evident to the endoscopist as redness,
may be the only alteration.
• Microscopy:
• In mild GERD the mucosal histology is often unremarkable. With more
significant disease, eosinophils are recruited into the squamous
mucosa, followed by neutrophils, which usually are associated with
more severe injury.
Basal zone hyperplasia exceeding 20% of the total epithelial thickness and elongation
of lamina propria papillae, such that they extend into the upper third of the
epithelium, also may be present.
34. 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.
35. Treatment
• Treatment with proton pump inhibitors or H2
histamine receptor antagonists, which reduce
gastric acidity, typically provides
symptomatic relief.
37. Chemical & Infectious esophagitis
Chemicals: Acids, alkalies, hot fluids, heavy smocking,
Medicinal pills. Iatrogenic esophageal injury may be caused
by cytotoxic chemotherapy, radiation therapy, or graft-versus host
disease.
Infectious esophagitis caused by: Bacterial, viral or fungal infections.
Esophagitis due to chemical injury generally causes only self-limited pain, particularly
odynophagia (pain with swallowing).Hemorrhage, stricture (narrowing), or perforation
may occur in severe cases.
38. Eosinophilic esophagitis
The incidence of eosinophilic esophagitis is increasing markedly.
Symptoms: food impaction and dysphagia in adults and feeding intolerance or GERD-like
symptoms in children.
The cardinal histologic feature is epithelial infiltration by large numbers of eosinophils,
particularly superficially and at sites far from the gastroesophageal junction.
Their abundance can help to differentiate eosinophilic esophagitis from GERD, Crohn disease,
and other causes of esophagitis.
Certain clinical characteristics, particularly failure of high-dose proton pump inhibitor
treatment and the absence of acid reflux, are also typical.
A majority of persons with eosinophilic esophagitis are atopic (having allergy), and many have atopic
dermatitis, allergic rhinitis, asthma, or modest peripheral eosinophilia.
Treatments include dietary restrictions to prevent exposure to food allergens, such as cow
milk and soy products, and topical or systemic corticosteroids.
