DISORDERS OF THE

ESOPHAGUS
ANATOMY OF THE ESOPHAGUS

• Hollow muscular tube guarded by

upper and lower sphincters
• Extends from the lower border of the
cricoid (C6) to the stomach
• The length- 25 to 30 cm.
• Viewed endoscopically- 15 cm. from
the teeth till 40 cm. at cardio-
esophageal junction
The middle of the esophagus-
open tubular view, pink
coloration. Sweeping wave like
contractions are what move
food
ANATOMY OF THE ESOPHAGUS

• Posterior mediastinum
• Diaphragmatic hiatus in front of the aorta
• Cervical esophagus best approached in the
left side of the neck
• Middle thoracic esophagus- approached by
right thoracotomy
• Distal esophagus-approached by left
thoracotomy
ANATOMY OF THE ESOPHAGUS

• Cardia = gastr-esoph. junction, the

junctional zone between pale
squamous esophageal mucosa and
pink gastric mucosa, Z line
• Up to 3 cm. of gastric mucosa type
extending up the esophagus is
accepted as normal
• More than that indicates Barret’s
esophagus
ASSESSMENT OF ESOPHAGEAL
DISEASE

• Careful history

• Physical examination

• Appropriate investigations
SYMPTOMS OF ESOPHAGEAL
DISEASE
• Dysphagia- difficulty in swallowing
• May be due to- organic disease (benign
strictures or esophageal carcinoma)
- esophagal motility disorders (achalasia
or diffuse esophageal spasm)
• Dysphagia for solids implies severe
disease, organic or functional
• Dysphagia for liquids- motility disorders
SYMPTOMS OF ESOPHAGEAL
DISEASE
• Regurgitation- effortless return of the
gastric content into the mouth
• Postural regurgitation is a common
symptom in reflux disease
• Precipitated by meals and increased in
intraabdo.pressure
• Overflow regurgitation into the
pharynx-trachea- aspiration
pneumonitis
SYMPTOMS OF ESOPHAGEAL
DISEASE
• Odynophagia- painful swallowing- organic
disease- esophagitis
• Esophageal pain- two sorts: heartburn and
angina-like tightening pain
• Heartburn is due to reflux of gastric juice to the
esophagus- esophagitis
• Angina-like tightening pain-esophageal anterior
chest pain, simulates angina pectoris- reflux
esophagitis, motility disorders
 Atypical Presentation of
Esophageal Disease
• Anemia due to chronic blood loss- erosive
esophagitis
• Acute upper GI bleeding- Mallory-Weiss
sdr.,peptic ulcer in a hiatus hernia
• Severe sepsis, respiratory distress-
perforation of the esophagus
• Angina-like pain- reflux disease
• Pulmonary symptoms- aspiration
pneumonitis- reflux disease
ESOPHAGEAL DISEASE
PHYSICAL SIGNS

• Inaccesible to physical examination

• Evidence of weight loss
• Palor due anemia
• Neck swelling
• Chest signs
• Hepatomegaly
ESOPHAGEAL DISEASE
INVESTIGATIONS
• CXR, Barium swallow, CT scan
• USS, external, endoscopic
• Radioisotope studies- labelled bollus
• Endoscopy with biopsy, cytology
• Manometry
• Ph 24-hours monitoring
• Tests to exclude cardiac disease- ecg,
coronary angiography
ESOPHAGEAL DISEASE
INVESTIGATIONS

• CXR may reveal:

- aspiration pneumonitis,
- mediastinal widening,
- fluid/gas level,
- mediastinal emphysema,
- pleural effusion
ESOPHAGEAL DISEASE
INVESTIGATIONS

• Barium swallow- indications

– Esophageal motility disorders
– Esophageal carcinoma and benign stricture
– Gastro-esophageal reflux +/- hiatus hernia
– Suspected esophageal perforation
– Leaking esophageal anastomosis
ESOPHAGEAL DISEASE
INVESTIGATIONS

• CT scan- preop.assessment of
esophageal malignancy
- extent of mural invasion,
- involvement of adjacent
structures,
- mediastinal lymph nodes
ESOPHAGEAL DISEASE
INVESTIGATIONS

• Radioisotope studies- assess g-e

incompetence:
- in pts. with reflux symptoms
- esophageal transit of liquid and
solid boluses in pts. with motility
disorders
ESOPHAGEAL DISORDER
INVESTIGATIONS

• Endoscopy- essential in all pts.with

dysphagia
– visual information- severity of
esophagitis
– esophageal cancer- biopsy, cytology
– gastro-esophageal reflux
ESOPHAGEAL DISEASE
INVESTIGATIONS

• Physiological tests
– manometry- the pressure profile-
motility disorders
– 24h.pH monitoring- pathological reflux is
considered when the time in the acid
zone Ph<4 is more than 5 min.
ESOPHAGEAL MOTILITY
DISORDERS

• Cricopharyngeal dysfunction

• Achalasia

• Diffuse esophgeal spasm

CRICOPHARYNGEAL
DISFUNCTION
• Failure of the UES to relax properly
• Pharyngoesofageal diverticulum- Zenker’s
• False diverticulum- mucosa herniates
posteriorly between the fb.of CPH.muscle
• Frequently associated with hiatus hernia
and GER.
• Symptoms: dysphagia, mass in the neck,
tracheal compression
CRICOPHARYNGEAL
DYSFUNCTION

• Diagnosis:
– history
– physical examination
– barium swollow
– endoscopy
CRICOPHARYNGEAL
DYSFUNCTION

• Treatment:
– Cricopharyngeal myotomy
– Excision of the diverticulum+myotomy
Formation of pharyngoesophageal (Zenker's) diverticulum.
Left- herniation of the pharyngeal mucosa and submucosa
occurs at the point of transition (arrow) between the oblique
fibers of the thyropharyngeus muscle and more horizontal
fibers of the cricopharyngeus muscle (Killian's triangle).
Center and right— as the diverticulum enlarges, it dissects
toward the left side and downward in the superior
mediastinum in the prevertebral space.
Barium swallow- Zenker’s
diverticulum
ACHALASIA

• Unknown etiology
• Abnormal peristalsis in the body of the esophagus,
resulting in:
– high resting LES pressure
– failure of the LES to relax during swollowing
The body of the esophagus becomes dilated
Carcinoma of the esophagus is 10 times commoner
in pts. with achalasia
ACHALASIA

• Symptoms:
– Difficulty in swollowing fluids
– Respiratory symptoms
– Vomiting
– Retrosternal pain
– Weight loss
ACHALASIA

• Diagnosis:-contrast studies- smooth

tapering narrowing of lower esoph. end
with dilated, tortuous lower esophagus,
uncoordinated or absent peristalsis
• Esophageal manometry
• Esophagoscopy
ACHALASIA

• Treatment:
– Non surgical treatment- pneumatic
dilatation of the LES
– Surgical- esophagomyotomy (Heller’s op.)
• Myotomy is confined to the lower portion of the
esophagus, 7-10 cm. and upper gastric muscle
• Esophagomyotomy can be combined with an
antireflux procedure
TREATMENT

• As the degenerative neural lesion of this

disease cannot be corrected, treatment is
directed at palliation of symptoms and
prevention of complications.

• Effective peristalsis is rarely restored by

successful treatment, but improved
oesophageal emptying and a decrease in
oesophageal diameter are generally expected.
Pharmacotherapy :

• Smooth muscle relaxants alleviate symptoms and

improve oesophageal emptying in up to 70% of
patients.
• Nitrites, such as sublingual isosorbide dinitrite,
and calcium channel blockers, such as diltiazem,
nifedipine and verapamil, have this effect.

• This treatment option is suitable for patients with

medical conditions that interfere with pneumatic
dilatation or myotomy.
Botulinum Toxin:

• Botulinum toxin type A is derived from the controlled

fermentation of Clostridium botulinum.
• The toxin binds to presynaptic cholinergic neuronal
receptors, interferes with acetylcholine release.
• Botulinum toxin decreases LOS basal tone and improves
symptoms in patients with achalasia.
• Beneficial response occurs in 90% of patients, but
symptoms reappear within a year in many initial
responders.
Dilatation:
• Forceful dilatation of the gastroesophageal sphincter to a
diameter of 3 cm is necessary to tear the circular muscle and
to ensure a lasting reduction in LOS pressure.
• Pneumatic dilators are conventionally used today.
• Water-soluble contrast material is used to detect distal
oesophageal leaks.
• Surgical consultation is undertaken if perforation is evident.
• Small perforations are managed conservatively with broad-
spectrum antibiotics.
• Clinical deterioration e.g. shock, sepsis, haemorrhage or a
finding of free-flowing barium into the mediastinum, requires
immediate thoracotomy and repair.
Dilatation

• At least 60% of patients have a good response

• The response rate varies with patient age, (younger
patients do not do as well as older patients), and
duration of symptoms, (those with a shorter history do
not respond as well)

• Morbidity is mostly related to oesophageal perforation,

a complication in approximately 5% of patients, but
surgical repair is required in less than half of these
cases.
Surgery:

• The Heller procedure was described in

1913 and now a modification of this
procedure is used most commonly in the
surgical management of achalasia

• An anterior myotomy is performed by

dividing the circular muscle of the
oesophagus down to the level of the
mucosa.
Minimally invasive surgical
procedures
• A preferable alternative to open myotomy, allowing the Heller
myotomy to be performed thoracoscopically and laparoscopically

• Shorter hospitalisation, less pain and early resumption of activity

are the benefits of the minimally invasive approach, which remains
as effective as the open techniques in the relief of dysphagia.

• Complications of minimally invasive surgery include: anterior

gastric perforation, mucosal perforation at the gastroesophageal
(GO) junction and, most significantly, GOR
Comparisons between
therapies

• Pneumatic dilatation, pharmacotherapy and botulinum

toxin injection are easy to use, usually well-tolerated
and relatively cheap treatment options in achalasia.
• Surgery generally gives longer-lasting results as well as
more complete relief of symptoms.
• Non-operative therapy is recommended initially.
Patients are only referred for surgery if they remain
symptomatic after 3 attempts at pneumatic dilatation.
a: Initial esophagram of patient with early achalasia and no
esophageal dilation.
b: Patient after 2 years of nonoperative treatment. Note
significant esophageal dilation and air-fluid level compared to
pretreatment.
c: End-stage achalasia with sigmoid or megaesophagus.
After satisfactory cardioesophageal myotomy, a
Toupet fundoplication is done- the posterior fundus
of the stomach is brought around the esophagus
and secured to the right crus and the right cut edge
of the myotomy. In a similar (in fact mirror image)
fashion the anterior fundus is sutured to the left
crus and left edge of the myotomy.
DIFFUSE ESOPHAGEAL
SPASM
• Strong nonperistaltic contractions
• Normal sphincter relaxation
• May be associated with GER
• Symptoms: chest pain
• Manometry-high amplitute repetitive contractions
• Constrast study: normal in ½, segmental spasm,
diverticula
DIFFUSE ESOPHAGEAL
SPASM

• Treatment:
– Surgery- long esophagomyotomy, from
the arch of the aorta to just above the
LES,-antireflux op in case of GER
– Medical treatment- calcium channel
blockers and smooth muscle relaxants
GASTRO-ESOPHAGEAL
REFLUX
• Secondary to LES dysfunction
• LES dysfunction may be related to:
– Decreased gastrin production
– Operation on or near the esophageal
hiatus
– Sliding hiatus hernia
– Scleroderma
– Tabacco and alcohol
GASTRO-ESOPHAGEAL
REFLUX
• Diagnosis:
• Substernal pain, heartburn,
regurgitation
• Manometry-decreased LES pressure
• Esopgagoscopy-esophagitis
• 24h pH monitoring
• Cineradiography
GERD-when acid from the
stomach bathes the lower
esoph. A feeling of heartburn
occurs.This can cause some
mild inflammation.
GERD- lower esoph. with a
slight erosion surrounded by
inflammed red tissue-
esophagitis gr.II
GERD- extensive deep
ulceration, severe case of
esophagitis (gr.III)
GERD- severe case of
extensive deep ulcerations in
the lower esoph
GASTRO-ESOPHAGEAL
REFLUX
• Treatment
– Medical: antiacids and metoclopramide
– Surgical: antireflux operations- Nissen
fundoplication- wrapping the lower esophagus
with gastric fundus
Indications for surgery:
-sy.refractory to medical treatment
-severe esophagitis, Barret’s esophagus
(replacement with columnar epithelium in the
lower esophagus secondry to esophagitis)
Barrett’s occurs after
longstanding reflux of acid.
The stomach lining grows up
where does not belong. Red
stomach tissue creeping up
Barrett’s- significant
progression
Barrett’s- extensive long
fingers and patches of
Barrett’s- prone to malignant
changes
 BARRETT’S ESOPHAGUS
• Replacement of the lower esophagus with
gastric-type mucosa, exceeding 3 cm. above
the squamo-columnar junction and gastric
mucosa islands amongst the squamous
mucosa
• Recognized as a metaplastic response to
reflux with increased exposure to gastric acid
• 30-fold increased risk of developing an
adenocarcinoma
• Regular endoscopic surveillance until an early
adenocarcinoma is detected