Esophageal disease

motility disorder
The word dysphagia is derived from the Greek phagia (to eat)
and dys (with difficulty). It specifically refers to the
sensation of food being hindered‫ تعوق‬in its normal passage
from the mouth to the stomach.
‫يشكل مرور الطعام عبر البلعوم إلى المريء‬
Glottis of larynx
 Dysphagia is defined as difficulty in swallowing.

 It may coexist with heartburn or vomiting but should be

distinguished from both .
 Make surer whether its true or pseudo dysphagia(globus
sensation or odynophagia):
I. globus sensation (in which anxious people feel a lump in the
throat without organic cause).
II. odynophagia (pain during swallowing, usually from gastro-
oesophageal reflux or candidiasis).
 CLASSIFICATION

Oropharyngeal dysphagia Esophageal dysphagia

Two distinct syndromes

Produced by abnormalities affecting Caused by the variety of

the finely tuned neuromuscular disorders affecting the smooth
mechanism of the striated muscle of muscle esophagus
the mouth, pharynx, and UES
Most causes are neurological (CN
lesion, stroke, cerebellar lesion)
Globus sensation
 Oropharyngeal disorders result from neuromuscular
dysfunction affecting the initiation of swallowing by the pharynx
and upper oesophageal sphincter.
 Chocking and regurgitation.

 Patients with oropharyngeal dysphagia have difficulty initiating

swallowing and develop choking, nasal regurgitation or tracheal
aspiration.
Other neurological manifestation:
 Drooling of saliva, dysarthria, hoarseness(vocal cord) and
cranial nerve or other neurological signs may be present.
Stricture, and Abnormal
fibrosis peristaltic
 Oesophageal causes include structural disease (benign or
malignant strictures) and dysmotility of the oesophagus.

 Patients with oesophageal disease complain of food 'sticking' after

swallowing, although the level at which this is felt correlates poorly
with the true site of obstruction.
 Usually the sticking is away from the site in which patient fells the
pain.
 Swallowing of liquids is normal until strictures become extreme.
(in esophageal structural abnormality)
 INVESTIGATIONS
 Dysphagia implies significant disease and should always be promptly
investigated.

 Endoscopy is the investigation of choice because it facilitates biopsy and

dilatation of suspicious strictures.

 If no abnormality is found, then barium swallow, with video fluoroscopic

swallowing assessment, will detect most motility disorders.

 In a few cases oesophageal manometry is required.

Spasm
scleroderma
 Progressive achalasia there is no
peristalsis so no motility.

Heartburn
Regurgitation
Bitter or sour taste in the mouth
Chest pain

The cricopharyngeal
(CP) bar can form from
a thickening of the
cricopharyngeal muscle Distal dysphagia
caused by replacement
of its muscle with
fibrous connective. This
is thought by many to be
a reaction to chronic
reflux of stomach
contents into the "Diffuse Esophageal
esophagus.
Spasm."
 PHARYNGEAL POUCH

 Incoordination of swallowing within the pharynx leads to

herniation through the cricopharyngeal muscle and
formation of a pouch.

 Most patients are elderly and have no symptoms, although

regurgitation, halitosis and dysphagia can occur. Some
notice gurgling in the throat after swallowing.

Herniation of esophagus through

the weak points
Bad odor from mouth caused by
food which remain in pouch
 Gurgling
Halitosis
Regurgitation
dysphagia
 A barium swallow demonstrates
 the pouch and reveals Incoordination
of swallowing, (be aware endoscopy
may cause perforation.) that’s why
Endoscopy may be hazardous.

 Surgical myotomy and resection of the

pouch are indicated in symptomatic
patients.
ACHALASIA OF THE OESOPHAGUS

Achalasia is a rare disease affecting 1:100 000 people. It

usually develops in middle life but can occur at any age.
 PATHOPHYSIOLOGY

Achalasia is characterised by:

 a hypertonic lower oesophageal sphincter which fails to relax

in response to the swallowing wave(vise versa to GERD)

 failure of propagated oesophageal contraction, leading to

progressive dilatation of the gullet.
 The cause is unknown.

 Defective release of nitric oxide by inhibitory

neurons in the lower oesophageal sphincter.

degeneration of ganglion cells within the

sphincter and the body of the oesophagus.
CLINICAL FEATURES

 The presentation is with dysphagia. This develops

slowly, is initially intermittent, and is worse for solids
and eased by drinking liquids, and by standing and
moving around after eating.

 Heartburn does not occur

 Some patients experience episodes of chest pain due

to oesophageal spasm.
 As the disease progresses, dysphagia worsens, the
oesophagus empties poorly and nocturnal pulmonary
aspiration develops.

 Achalasia predisposes to squamous carcinoma of the

oesophagus.
A barium swallow
shows tapered narrowing of
the lower oesophagus and in
late disease the oesophageal
body is dilated, aperistaltic
and food-filled.
Endoscopy should always be carried out because carcinoma of
the cardia can mimic the presentation and radiological and
manometric features of achalasia ('pseudo-achalasia’).
Difficulty in passing OF the endoscope but with air there is
Popping up (sudden insertion into stomach)
High resolution manometry
Achalasia subtypes stratify prevalent esophageal
body pressure patterns with:
1. subtype I, absent pressures (aperistalsis);
2. subtype II, uniform pressures (esophageal pan
pressurization);
3. subtype III, spasm pressures (spastic,
premature or abnormal contractions).
 High resolution manometry (HRM) confirms the high-
pressure, non-relaxing lower oesophageal sphincter with
poor contractility of the oesophageal body
Integrated Relaxation Pressure spastic
esophageal

pan esophageal
Dilatation MYOTOMY

Extremely High Panesophageal Pressurization

 MANAGEMENT
Endoscopic
 Forceful pneumatic dilatation using a 30-
35 mm diameter fluoroscopically positioned
balloon disrupts the oesophageal sphincter and
improves symptoms in 80% of patients.
 Endoscopically directed injection of
botulinum toxin into the lower oesophageal
sphincter induces clinical remission, but relapse
is common(6 months).
 POEM per oral endoscopic myotomy(third
space endoscopy)
 Incision of mucosa
 Submucosa cutter
 Muscle cutting
 Then close it(clips).
 Surgical
 Surgical myotomy ('Heller's operation'), performed either
laparoscopically or as an open operation, is an extremely
effective, although more invasive option.
OTHER OESOPHAGEAL MOTILITY DISORDERS

 Diffuse oesophageal spasm presents in late middle age with

episodic chest pain which may mimic angina,
 Treatment is based upon the use of PPI drugs when gastro-
oesophageal reflux is present. Oral or sublingual nitrates or
nifedipine may relieve attacks of pain.

 'Nutcracker' oesophagus is a condition in which extremely

forceful peristaltic activity leads to episodic chest pain and
dysphagia.
 Treatment is with nitrates or nifedipine.
SECONDARY CAUSES OF OESOPHAGEAL
DYSMOTILITY

 systemic sclerosis

 Dermatomyositis.

 rheumatoid arthritis .

 myasthenia gravis.
THANK YOU