‫بسم هللا الرحمن الرحيم‬

Esophagus
(structure, function, disorders)
Dr. Zeinab Helmy
Professor of internal Medicine
Structure of the esophagus:
 The esophagus is a hollow muscular tube that takes food and liquid from the
pharynx to the stomach (no digestion takes place here).
 It extends from the level of the lower border of the cricoid cartilage at the level of
the 6 th cervical vertebra (C6) to the cardiac orifice of the stomach at the level of T11
or T12.

 Peristalsis of the esophagus propels food in one direction (to the stomach) even if
the body is horizontal or upside down.
 The esophagus, which is 10-12 inches (25 -30cm) long, and has two sphincters that
control opening and closing.
 The upper third esophagus and the upper esophageal sphincter (UOS) (at C6) are
under voluntary control.
 At the junction with the stomach, the lumen of the esophagus is surrounded by a
circular smooth muscle which form the lower esophageal sphincter (LES, also
called the gastroesophageal or cardiac sphincter). The surface marking for this
point is the left seventh costal cartilage.
 The LES relaxes to permit food to enter the stomach, then contracts to prevent the
backup of stomach contents. It is 3-5 cm long, physiological sphincter.
 If the LES does not close completely, gastric juice may splash up into the
esophagus.
 It passes though the diaphragm at the level of the tenth thoracic vertebra (C10).
 4 cm of esophagus lies below the diaphragm. It is lined by

Endoscopic Anatomy of the esophagus:

 The narrowest point of the esophagus is the UOS, 15 cm from the incisors.
 The diaphragm at 38 cm.
 The gastro-esophageal junction is defined endoscopically as the upper margin of the
proximal gastric folds. On average this is at 37 cm in females and 40 cm in males.
 The squamocolumnar junction is also visible endoscopically as the Z-line and
usually overlaps with the gastro-esophageal junction.
Microscopic anatomy of esophagus:
1 Mucosa:
 Lined with nonkeratinized stratified squamous epithelium, rich in
glycogen.
 Lamina propria is a fibrovascular connective tissue
between epithelium and muscularis mucosae.
Muscularis mucosa: thin layer of longitudinal smooth muscle
2- Submucosa:
 Loose connective tissue with vessels, lymphatics, occasional
white blood cells, lymphoid follicles (rare),
Contains sparse ganglia and nerve.
3- Muscularis externa:
 Striated in the upper part and smooth in lower 2/3 (thus,
skeletal muscle disorders cause esophageal dysfunction).
 Inner circular and outer longitudinal layers.
 Contains Auerbach (myenteric)
plexus.
4 Adventitia.
 Loose connective tissue; no consistent serosa so tumors
and infections spread readily.
 No serosal covering.
 Constrictions:
The distance of each constriction is measured from the upper incisor teeth.
First constriction At the UOS (at C6) 9 cm (6 inches) from the incisor teeth.
Second constriction where it’s crossed by the 22.5 cm (9 inches) from the incisor
arch of aorta (at T4) teeth.
Third constriction where it’s crossed by the left 27.5 cm (11 inches) from the incisor
main bronchus (at T5-T6) teeth
Fourth constriction where it pierces the 40 cm (15 inches) from the incisor
diaphragm (at T10) teeth

CLINICAL IMPORTANCE OF ESOPHAGEAL CONSTRICTIONS:

 These are the sites where swallowed foreign bodies may stick in the
esophagus.
 These are the sites where strictures develop after ingestion of caustic
substances.
 These sites have predilection for the carcinoma of the esophagus.
 These are sites via which it might be difficult to pass gastric tube.

Eosophageal innervation:

The esophagus is innervated by the oesophageal plexus, which is formed by a

combination of the parasympathetic vagal trunks and sympathetic fibres.

Two different types of nerve fibre run in the vagal trunks.

The UOS and upper striated muscle is supplied by fibres originating from the
nucleus ambiguus.

Fibres supplying the LOS and smooth muscle of the lower oesophagus arise from the
dorsal motor nucleus.
Mechanism of LOS relaxation:
Transient LES relaxation is a neural reflex with afferent and efferent pathways.

The afferent stimuls originate in the pharynx by swallow.

Then, the afferent signals travel to the sensory nucleus (nucleus solitarius).

(A) Esophageal motor innervation by the vagus nerve; Auerbach’s and Meissner’s
plexuses.

(B)The striated muscle of the proximal esophagus is directly innervated by the

somatic efferent cholinergic fibers (Ach) of the vagus nerve originating from the
nucleus ambiguus. Mediates esophageal peristalsis and UOS relaxation.

In contrast, the smooth muscle of the distal esophagus is innervated by the

preganglionic vagus nerve fibers from the dorsal motor nucleus.

The preganglionic vagus fibers release ACh, that affects two types of postganglionic
neurons in the myenteric plexus, the excitatory cholinergic neurons and the inhibitory
nitrinergic neurons. NO and VIP are the postganglionic neurotransmitter responsible
for LES relaxation.
Symptoms of esophageal disorders:
Dysphagia:
Difficulty in swallowing of food only or food and fluid.
Odynophagia:
Pain on swallowing. Suggest inflamation and ulceration.
Heartburn:
Chest pain:
It is difficult to distinguish from cardiac pain.
Other important symptoms:
Loss of weight, anaemia, cachexia and change of voice.
 Dysphagia

Esophagus disorders:
1) Mallory-Weiss syndrome
2) Eosinophilic esophagitis
3) Esophageal Rings and Webs
4) Esophageal Diverticulum
5) GERD
6) Esophageal Varices
7) Benign esophageal neoplasm.
8) Esophageal Cancer
9) Esophageal motility disorders.
Esophagus Tests:
 Upper GIT endoscopy:
A flexible tube with a camera is inserted through the mouth. The endoscope
allows examination of the esophagus, stomach, and duodenum.
 Biopsy:
Done through an endoscope, a small piece of the esophagus is taken to be
evaluated under a microscope.
• Endoscopic ultrasound (EUS):
EUS is a procedure that combines endoscopy and ultrasound to capture high
quality images of the digestive tract. It is often used to diagnose Barrett’s
esophagus and stage esophageal cancer.
 Esophageal pH monitoring testing:
It is used to measure whether acid is escaping the stomach and flowing
backward into the esophagus. Monitoring pH can help identify GERD and
follow the response to treatment.
1 Traditional esophageal pH testing, a catheter containing a sensor that
detects acid is passed through your nose and down into your esophagus,
where it remains for 24 hours.
2 Wireless esophageal pH testing, a small capsule is placed on the wall of
your esophagus via a catheter. Once the catheter is removed, the device
wirelessly transmits pH measurements to a receiver worn at your waist.
 High-resolution esophageal manometry:
It is a procedure that measures how the muscles in the esophagus contract
and relax after swallow, which is an indication of the esophagus is functioning.
It is the gold standard for diagnosing motility disorders.
 Barium swallow:
A person swallows a barium solution, then X-ray films are taken of the
esophagus and stomach. Most often, a barium swallow is used to seek the cause
of difficulty swallowing.
 Fiberoptic endoscopic evaluation of swallowing (FEES):
It is used to test swallowing function. A camera attached to a catheter is placed
in your throat, where it records what happens when you swallow food.

Esophagus disease treatments

 Medication:
1. H2 blockers: Histamine stimulates acid release in the stomach. Certain
antihistamines called H2 blockers can reduce acid, improving GERD and
esophagitis.
2. Proton pump inhibitors: These medicines turn off many of the acid-
producing pumps in the stomach wall. Reduced stomach acid can
reduce GERD symptoms, and help ulcers or esophagitis to heal.

 Esophageal balloon dilation:

A balloon is passed down the esophagus and inflated to dilate a
stricture, web, or ring that interferes with swallowing.

 Laparoscopic Heller myotomy:

It is a minimally-invasive surgical procedure used to treat achalasia.

 Minimally invasive esophagectomy:

It is a surgical procedure that removes part or all of the esophagus.
After
it is removed, the esophagus is rebuilt from part of stomach or part of large
intestine. This procedure is usually reserved for patients who have
Barrett’s esophagus or esophageal cancer.
 Cryoablation (cryotherapy):
It is often used to treat Barrett’s esophagus or early-stage esophageal
cancer. During the procedure, a liquid nitrogen spray is used to freeze and
kill pre-cancerous or cancerous lesions inside the esophagus.
 Radiofrequency ablation (RFA) therapy:
It is also used to treat Barrett’s esophagus. It uses thermal energy to burn
and kill pre-cancerous lesions.
 Endoscopic mucosal resection:
It is a procedure that removes abnormal or cancerous tissue from the
esophagus.
 Minimally-invasive fundoplication, anti-reflux surgery, is a treatment for
GERD.
 Esophageal variceal banding:
During endoscopy, rubber band-like devices can be wrapped around
esophageal varices. Banding causes varices to clot, reducing their chance
of bleeding.
 Confocal laser endomicroscopy:
A new procedure that takes the microscope inside a patient, which
may replace the need for many biopsies.

Mallory-Weiss syndrome (MWS)

Mallory-Weiss syndrome is characterized by upper gastrointestinal bleeding
secondary to longitudinal mucosal tear at the gastroesophageal junction or gastric
cardia.
It is more common in males than in females.
It occurs more often in people with alcoholism.
The people between the ages of 40 and 60 are more likely to develop MWS. However,
there are cases of Mallory-Weiss tears in children and young adults.

Causes:
 Severe or prolonged vomiting.
 Trauma to the chest or abdomen.
 Severe or prolonged hiccups.
 Intense coughing
 Heavy lifting or straining.
 Gastritis.
 hiatal hernia.
 Convulsions.
Symptoms:
 Abdominal pain
 Hematemesis
 Involuntary retching
 Black stools

Investigations:
 CBC
 Upper GIT endoscopy.

Treatment:
1. The bleeding was stop on its own in about 80 to 90 % of MWS cases.
2. Healing typically occurs in a few days and doesn’t require treatment.
3. But if the bleeding doesn’t stop, the patients may need one of the following
treatments:

Endoscopic therapy:
 Injection therapy, which delivers medication to the tear to stop the bleeding.
 Coagulation therapy, which delivers heat to seal off the torn vessel.

Surgical:
Sometimes, endoscopic therapy isn’t enough to stop the bleeding, so other
ways of stopping the bleeding must be used, such as laparoscopic surgery.

Medication:
Medications to reduce stomach acid production.
 Esophageal motility
disorders
Classification of Esophageal motility disorders

[I] Primary esophageal motility disorders [II] Secondary esophageal motility disorders
Inadequate LES relaxation:
 Classic achalasia.
 Atypical disorders of LES relaxation.

Uncoordinated contraction:
 Diffuse esophageal spasm.

Hypercontraction:
 Nutcracker esophagus
 Isolated hypertensive LES

Hypocontraction:
 Ineffective esophageal motility

Another classification
 Achalasia
Definition:
It is a primary motor disorder of the esophagus of unknown etiology, characterized
monometrically by incomplete relaxation of the LES and loss of esophageal peristalsis in the
lower 2/3, leading to accumulation of food.

It is common among the middle-aged and old people. Males are at a greater risk of
developing than females. prevalence that ranges up to 1 per 10,000 persons. There is no racial
predilection.
Symptoms:
1. The hallmark symptom of achalasia is gradual onset and long standing of
dysphagia for solid and liquid.
2. Regurgitation of undigested food during meal up to several hours,
unresponsive to initial trial of proton pump inhibitor (PPI) therapy (76 to 91%).
3. Retrosternal discomfort after eating.
4. Substernal chest pain not related to food or exercise in 50% of patients.
5. Cough during night duo to night regurgitation.
6. even heartburn may be accompanying symptoms that often lead to
misdiagnosis of achalasia erroneously as gastroesophageal reflux disease.
7. Weight loss.

Causes and Pathophysiology:

Achalasia is mainly caused by progressive neuronal damage in the
myenteric plexus, which results in a nonrelaxing, hypertensive LES and
aperistalsis of the body of the esophagus.
The exact cause of the neuronal degeneration is not yet understood.
Diagnosis of achalasia:
 Esophageal manometry:
Absent peristalsis
High LES pressure
Failure of relaxation of
LES.
 Radiographic studies
 Endoscopy to exclude
organic disease

TREATMENT OF ACHALASIA
 Medical: Smooth muscle
relaxants
 Balloon Dilatation
 Surg ical myotomy

Complications

As the condition progresses, individuals may find it extremely difficult to ingest

food and water. They tend to avoid eating and drinking to prevent pain and
discomfort. This leads to malnutrition and weight loss.
Achalasia can also lead to pneumonia and lung infections, caused by aspiration of
food, especially in the elderly people.

Achalasia is also known to increase the risk of esophageal cancer. Regular cancer
screening is warranted in patients with achalasia.