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,
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