Esophagus - anatomic and physiologic data,

research methods, diseases, clinic,

treatment
 The oesophagus
• The oesophagus is a fibromuscular tube,
approximately 25cm in length, that
transports food from the pharynx to
the stomach.
• It originates at the inferior border of
the cricoid cartilage (C6) and extends to
the cardiac orifice of the stomach (T11).
• The oesophagus begins in the neck, at the
level of C6. Here, it is continuous
superiorly with the laryngeal part of
the pharynx (the laryngopharynx).
• It descends downward into the superior
mediastinum of the thorax, positioned
between the trachea and the vertebral
bodies of T1 to T4. It then enters the
abdomen via the oesophageal hiatus (an
opening in the right crus of the
diaphragm) at T10.
• The abdominal portion of the oesophagus
is approximately 1.25cm long – it
terminates by joining the cardiac orifice of
the stomach at level of T11.
Muscular layers
The oesophagus consists of an internal circular layer and an external longitudinal layer of muscle.
Furthermore, the external longitudinal layer is composed of different muscle types in each third
of the oesophagus:
• Superior third – voluntary striated muscle
• Middle third – voluntary striated and smooth muscle
• Inferior third – smooth muscle
Food is transported through the
oesophagus by peristalsis –
a rhythmic contractions of the
muscles, which propagates
down the oesophagus.
Hardening of these muscular layers
can interfere with peristalsis and cause
 difficulty in swallowing (dysphagia).
 Oesophageal Sphincters
There are two sphincters present in the oesophagus, known as the upper and
lower oesophageal sphincters. They act to prevent the entry of air and the
reflux of gastric contents respectively.
Upper Oesophageal Sphincter
The upper sphincter is an anatomical,
striated muscle sphincter at the
junction between the pharynx and
oesophagus. It is produced by the 
cricopharyngeus muscle. Normally,
it is constricted to prevent the
entrance of air into the oesophagus.
Lower Oesophageal Sphincter
The lower oesophageal sphincter is a physiological sphincter located in the gastro-
oesophageal junction. Wich is situated to the left of the T11 vertebra, and is marked by
the change from oesophageal to gastric mucosa.
• The sphincter is classified as a physiological (or functional) sphincter, as it does not have
any specific sphincteric muscle. Instead, the sphincter is formed from four phenomena:
• The oesophagus enters the stomach at an acute angle.
• The walls of the intra-abdominal section of the oesophagus are compressed when there
is a positive intra-abdominal pressure.
• The folds of mucosa present aid in occluding the lumen at the gastro-oesophageal
junction.
• During oesophageal peristalsis, the sphincter is relaxed to allow food to enter the
stomach. Otherwise at rest, the function of this sphincter is to prevent the reflux of
acidic gastric contents into the oesophagus.
 Vasculature
The thoracic part of the oesophagus receives its arterial
supply from the branches of the thoracic aorta and
the inferior thyroid artery (a branch of the thyrocervical
trunk). Venous drainage into the systemic circulation
occurs via branches of the azygous veins and the inferior
thyroid vein.

The abdominal oesophagus is supplied by the left gastric

artery (a branch of the coeliac trunk) and left inferior
phrenic artery. This part of the oesophagus has a mixed
venous drainage via two routes:
• To the portal circulation via left gastric vein
• To the systemic circulation via the azygous vein.
These two routes form a porto-systemic anastomosis, a
connection between the portal and systemic venous
systems.
 Innervation
• The oesophagus is innervated by
the oesophageal plexus, which is formed by
a combination of the parasympathetic vagal
trunks and sympathetic fibres from
the cervical and thoracic sympathetic
trunks.
• Two different types of nerve fibre run in the
vagal trunks. The upper oesophageal
sphincter and upper striated muscle is
supplied by fibres originating from
the nucleus ambiguus. Fibres supplying the
lower oesophageal sphincter and smooth
muscle of the lower oesophagus arise from
the dorsal motor nucleus.
Lymphatics

• The lymphatic drainage of
the oesophagus is divided
into thirds:
• Superior third – deep
cervical lymph nodes.
• Middle third – superior and
posterior mediastinal nodes.
• Lower third – left gastric
and celiac nodes.
Physiology
The main function of the oesophagus is to transfer food from the mouth
to the stomach in a coordinated fashion. The initial movement from the
mouth is voluntary. The pharyngeal phase of swallowing involves
sequential contraction of the oropharyngeal musculature, closure of the
nasal and respiratory passages, cessation of breathing and opening of
the upper oesophageal sphincter. Beyond this level, swallowing is
involuntary. The body of the oesophagus propels the bolus through a
relaxed lower oesophageal sphincter (LOS) into the stomach, taking air
with it. This coordinated oesophageal wave that follows a conscious
swallow is called primary peristalsis. It is under vagal control, although
there are specific neurotransmitters that control the LOS.
The upper oesophageal sphincter is normally closed at rest and serves as
a protective mechanism against regurgitation of oesophageal contents
into the respiratory passages. It also serves to stop air entering the
oesophagus other than the small amount that enters during swallowing.
The LOS is a zone of relatively high pressure that prevents gastric
contents from refluxing into the lower oesophagus. In addition to
opening in response to a primary peristaltic wave, the sphincter also
relaxes to allow air to escape from the stomach and at the time of
vomiting. A variety of factors influence sphincter tone, notably food,
gastric distension, gastrointestinal hormones, drugs and smoking
• Dysphagia is used to describe difficulty with
swallowing.
• Odynophagia refers to pain on swallowing.
• Regurgitation and reflux often used
synonymously. It is helpful to differentiate
between them, although it is not always
possible. Regurgitation should strictly refer
to the return of oesophageal contents from
above a functional or mechanical
obstruction. Reflux is the passive return of
gastroduodenal contents to the mouth as
part of the symptomatology of
gastrooesophageal reflux disease (GORD).
Chest pain
Chest pain similar in character to angina pectoris may arise from an
oesophageal cause, especially gastro-oesophageal reflux and motility
disorders. Exercise-induced chest pain can be due to reflux;
Symptoms of oesophageal disease:
■ Difficulty in swallowing described as food or fluid sticking (oesophageal
dysphagia) must rule out malignancy
■ Pain on swallowing (odynophagia) suggests inflammation and ulceration
■ Regurgitation or reflux (heartburn) common in gastrooesophageal reflux
disease
■ Chest pain is difficult to distinguish from cardiac pain
 Investigations
Radiography:
Contrast radiography has been somewhat overshadowed by
endoscopy but remains a useful investigation for
demonstrating narrowing, space-occupying lesions,
anatomical distortion or abnormal motility. An adequate
barium swallow should be tailored to the problem under
investigation. It may be helpful to give a solid bolus (bread
or marshmallow) if a motility disorder is suspected.
CT scann.
Cross-sectional imaging by computed tomography (CT)
scanning is an essential investigation in the assessment of
neoplasms of the oesophagus and can be used in place of a
contrast swallow to demonstrate perforation.
 Endoscopy
Endoscopy is necessary for the investigation of most oesophageal
conditions. It is required to view the inside of the oesophagus and the
oesophagogastric junction, to obtain a biopsy or cytology specimen, for the
removal of foreign bodies and to dilate strictures. There are two types of
instrument available, the rigid oesophagoscope and the flexible video
endoscope, but the rigid instrument is now virtually obsolete. Novel
techniques that rely on fluorescence and narrow band imaging to enhance
visual contrast are becoming increasingly used for the identification of
mucosal abnormalities that are not easily seen with white light, for instance
in patients with Barrett’s oesophagus undergoing endoscopic surveillance.
As a matter of routine, the stomach and duodenum are examined as well as
the oesophagus. If a stricture is encountered, it may be helpful to dilate it to
allow a complete inspection of the upper gastrointestinal tract.
Endosonography
Endoscopic ultrasonography relies on a high-frequency (5–30 MHz)
transducer located at the tip of the endoscope to provide highly
detailed images of the layers of the oesophageal wall and mediastinal
structures close to the oesophagus. Radial echoendoscopes have a
rotating transducer that creates a circular image with the endoscope in
the centre, and this type of scanner is widely used to create diagnostic
transverse sectional images at right angles to the long axis of the
oesophagus. Linear echoendoscopes produce a sectoral image in the
line of the endoscope and are used to biopsy submucosal oesophageal
lesions or mediastinal masses such as lymph nodes.
Oesophageal manometry
Manometry is widely used to diagnose
oesophageal motility disorders.
Recordings are usually made by passing a
multilumen catheter with three to eight
recording orifices at different levels down
the oesophagus and into the stomach.
High-resolution manometry uses a
multiple (up to 30) microtransducer
catheter with the results displayed as
spaciotemporal plots; this system is likely
to supplant conventional manometry.
Twenty-four hour pH and combined pH-
impedance recording
Prolonged measurement of pH is
now accepted as the most
accurate method for the
diagnosis of gastro-oesophageal
reflux. It is particularly useful in
patients with atypical reflux
symptoms, those without
endoscopic oesophagitis and
when patients respond poorly to
intensive medical therapy.
Diseases of the Esophagus

• Achalasia
• Barrett's Esophagus
• Esophageal Cancer
• Gastroesophageal Reflux Disease (GERD)
• Peptic Stricture
• Webs, Rings and Diverticula
Achalasia
Achalasia is a motor
disorder characterized by
a complete loss of
contraction and relaxation
of muscles used to move
contents down the
esophagus. It is due to
loss of the ganglion cells
in the myenteric
(Auerbach’s) plexus.
Pathophysiology.
Achalasia is an esophageal disease of unknown etiology, although it
may be secondary to ganglionic dysfunction, which causes:
(1) High resting LES pressure
(2) Failure of the LES to relax during swallowing
(3) Absence of coordinated peristalsis in the body of the esophagus
b. The body of the esophagus becomes dilated, and the muscle
hypertrophies in an attempt to force material through the dysfunctional
LES. A similar symptom complex can be caused by Chagas disease,
which is caused by the organism Trypanosoma cruzi.
c. Carcinoma of the esophagus is 10 times more common in patients
with achalasia than in the general population.
Symptoms of achalasia include dysphagia,
followed by regurgitation and weight loss.
Frequently, respiratory symptoms caused by
aspiration are present.
3. Diagnosis
a. Radiographic studies reveal a dilated
esophagus with a bird's beaklike extension
into the lower narrowed segment at the LES.
b. Esophageal manometry reveals the high resting
LES pressure, failure of relaxation during
swallowing, higher than normal resting pressure
in the body of the esophagus, and absence of
peristalsis.
c. Esophagoscopy is required to rule out neoplasia
and to document the extent of esophagitis.
Treatment for achalasia is palliative because LES function can never be restored to
normal.
a. Nonsurgical treatment consists of forced pneumatic dilatation of the spastic
lower esophageal sphincter, which is just above the gastroesophageal junction.
b. b. Surgical treatment is esophagomyotomy by the modified Heller procedure,
via laparotomy! laparoscopy, or occasionally left thoracotomy. Care is taken
not to disturb the vagus nerve attachments to the esophagus to prevent reflux.
The myotomy is confined to the lower portion of the esophagus, usually 6-8
cm in length.
(I) Surgical results with the Heller procedure are generally better than with
pneumatic dilatation for relief of dysphagia.
Barrett's Esophagus
• Barrett’s oesophagus is a metaplastic change in the lining mucosa of
the oesophagus in response to chronic gastrooesophageal reflux
 GASTRO-OESOPHAGEAL REFLUX
DISEASE
Gastroesophageal reflux disease (GERD)
is a chronic digestive disorder where
liquid content from the stomach backs
up into the esophagus, with the most
common symptom being heartburn.
The classical triad of symptoms is
retrosternal burning pain (heartburn),
epigastric pain (sometimes radiating
through to the back) and regurgitation.
 PERFORATION
Perforation of the oesophagus is usually iatrogenic (at
therapeutic endoscopy) or due to ‘barotrauma’
(spontaneous perforation-Boerhaave syndrome) This
occurs classically when a person vomits against a closed
glottis. The pressure in the oesophagus increases
rapidly, and the oesophagus bursts at its weakest point
in the lower third, sending a stream of material into the
mediastinum and often the pleural cavity as well.
The diagnosis can usually be suspected from the history
and associated clinical features. A chest x-ray is often
confirmatory with air in the mediastinum, pleura or
peritoneum. Pleural effusion occurs rapidly either as a
result of free communication with the pleural space or
as a reaction to adjacent inflammation in the
mediastinum. A contrast swallow or CT is nearly always
required to guide management
Treatment of oesophageal perforations
Perforation of the oesophagus
usually leads to mediastinitis. The
loose areolar tissues of the
posterior mediastinum allow a
rapid spread of gastrointestinal
contents. The aim of treatment is
to limit mediastinal contamination
and prevent or deal with infection.
non-operative treatment aims to
limit the effects of mediastinitis
and provide an environment in
which healing can take place.
The decision between operative and non-operative management rests on
four factors. These are:
1. the site of the perforation (cervical versus thoracoabdominal
oesophagus);
2. the event causing the perforation (spontaneous versus instrumental);
3. underlying pathology (benign or malignant);
4 the status of the oesophagus before the perforation (fasted and empty
versus obstructed with a stagnant residue). It follows that most
perforations that can be managed nonoperatively occur in the context of
small instrumental perforations of a clean oesophagus without
obstruction.
 MALLORY–WEISS SYNDROME
Forceful vomiting may produce a mucosal tear at
the cardia rather than a full perforation. The
mechanism of injury is different. In Boerhaave’s
syndrome, vomiting occurs against a closed
glottis, and pressure builds up in the oesophagus.
In Mallory– Weiss syndrome, vigorous vomiting
produces a vertical split in the gastric mucosa,
immediately below the squamocolumnar junction
at the cardia in 90 percent of cases. In only 10
percent is the tear in the oesophagus. The
condition presents with haematemesis.
NEOPLASMS OF THE OESOPHAGUS

Benign tumours
Benign tumours of the oesophagus are relatively rare. True papillomas,
adenomas and hyperplastic polyps do occur, but the majority of
‘benign’ tumours are not epithelial in origin and arise from other layers
of the oesophageal wall (gastrointestinal stromal tumour (GIST),
lipoma, granular cell tumour). Most benign oesophageal tumours are
small and asymptomatic, and even a large benign tumour may cause
only mild symptoms. The most important point in their management is
usually to carry out an adequate number of biopsies to prove beyond
reason.
 Malignant tumours
• Non-epithelial primary malignancies are also rare, as is malignant
melanoma. Secondary malignancies rarely involve the oesophagus
with the exception of bronchogenic carcinoma by direct invasion of
either the primary and/or contiguous lymph nodes.
• Cancer of the oesophagus is the sixth most common cancer in the
world. In general, it is a disease of mid to late adulthood, with a poor
survival rate. Only 5–10 per cent of those diagnosed will survive for
five years.
The exact cause is
unknown. Associated
factors are tobacco use,
excessive alcohol
ingestion, nitrosamines,
poor dental hygiene, and
hot beverages. Certain
pre-existing conditions
also increase the
likelihood of developing
esophageal cancer,
including achalasia and
Barrett's esophagus.
Pathology:
Type
(1) Squamous cell carcinoma is the most common form.
(2) Adenocarcinoma, the next commonest, is the type that occurs in
patients with Barrett's esophagus.
(3) Rare tumors of the esophagus include mucoepidermoid carcinoma and
adenoid cystic carcinoma.
Tumor spread.
Esophageal malignancies metastasize through both the lymphatic system
and the bloodstream, with metastases occurring in liver, bone, and brain.
Tumor spread.
Esophageal malignancies metastasize through both the lymphatic system
and the bloodstream, with metastases occurring in liver, bone, and brain.
Diagnosis
a. A history of dysphagia and weight loss is almost always present.
b. Contrast study of the esophagus demonstrates the location and extent of the
tumor.
c. Computed tomography ( CT) scan of the chest and abdomen is done to evaluate
local lymphatic spread, and a thorough search is made for distant metastases.
d. Esophagoscopy is essential for tissue diagnosis and determination of the extent
of the tumor.
e. EUS is done to assess the depth of the invasion and staging.
f. Bronchoscopy is performed in patients with proximal esophageal lesions to
assess the possibility of invasion of the tracheobronchial tree.
 Treatment
a. Overall, surgical therapy is associated with
less than a 5% mortality rate. Several
procedures are described for resection of
the esophagus. Transhiatal esophagectomy
through a laparotomy and cervical
incisions. A complete thoracic
esophagectomy is performed bluntly with
reconstruction of gastrointestinal continuity
with the stomach or, rarely, the colon.
b. Ivor Lewis esophagectomy through a right
thoracotomy and laparotomy.
Reconstruction is also accomplished with
the stomach or, rarely, the colon.
Radiotherapy and chemotherapy are currently being investigated as
adjuncts to surgery or as primary treatment modalities.
(1) Neoadjuvant chemotherapy in combination with X-Ray Therapy (XRT)
given before surgical resection appears to shrink the tumor mass.
Several studies have shown an impact on long-term survival.
Combination chemotherapy with cisplatin have shown up to a 50%
response rate. However, a significant long-term survival has not been
demonstrated.
(2) Radiotherapy alone for carcinoma of the esophagus results in a 5-year
survival of less than 10%.
(3) In patients who have advanced disease with either invasion of the
tracheobronchial tree or advanced metastases, palliative effects may be
obtained by utilizing endoscopically placed metallic stents to allow
swallowing of saliva and soft foods.
MOTILITY DISORDERS AND
DIVERTICULA
A motility disorder can be readily understood when a patient has
dysphagia in the absence of a stricture, and a barium impregnated food
bolus is seen to stick in the esophagus. If this can be correlated with a
specific abnormality on esophageal manometry, accepting that this is
the cause of the patient’s symptoms may be straightforward.
Unfortunately, this is often not the case. Pain, with or without a
swallowing problem, is frequently the dominant symptom, and patients
often undergo extensive hospital investigation before the esophagus is
considered as a source of symptoms.
Pharyngeal and oesophageal diverticula
Most oesophageal diverticula are pulsion diverticula that develop at a site of weakness as
a result of chronic pressure against an obstruction. Symptoms are mostly caused by the
underlying disorder unless the diverticulum is particularly large. Traction diverticula are
much less common. They are mostly a consequence of chronic granulomatous disease
affecting the tracheobronchial lymph nodes due to tuberculosis, atypical mycobacteria or
histoplasmosis. Fibrotic healing of the lymph nodes exerts traction on the oesophageal
wall and produces a focal outpouching that is usually small and has a conical shape. There
may be associated broncholithiasis, and additional complications may occur, such as
aerodigestive fistulation and bleeding
Zenker’s diverticulum (pharyngeal pouch)
Is not really an oesophageal diverticulum as it protrudes posteriorly above the
cricopharyngeal sphincter through the natural weak point (the dehiscence of
Killian) between the oblique and horizontal (cricopharyngeus) fibres of the
inferior pharyngeal constrictor. The exact mechanism that leads to its
formation is unknown, but it involves loss of the coordination between
pharyngeal contraction and opening of the upper sphincter. When the
diverticulum is small, symptoms largely reflect this incoordination with
predominantly pharyngeal dysphagia. As the pouch enlarges, it tends to fill
with food on eating, and the fundus descends into the mediastinum.
Treatment can be undertaken endoscopically with a linear cutting stapler to
divide the septum between the diverticulum and the upper oesophagus,
producing a diverticulo-oesophagostomy, or can be done by open surgery.
Schatzki’s ring
Schatzki’s ring is a circular ring in the distal oesophagus usually at the
squamocolumnar junction. The cause is obscure, but there is a strong
association with reflux disease. The core of the ring consists of variable
amounts of fibrous tissue and cellular infiltrate. Most rings are incidental
findings. Some are associated with dysphagia and respond to dilatation in
conjunction with medical antireflux therapy.