1.
PROFESSOR CONSULTANT
SURGEON DR. ALI
AL- TAEY

2.
CLINICAL FEATURES OF OESOPHAGEAL DISEASES
• What is odynophagia?
• Pain on swallowing
• primary peristalsis?
• Coordinated oesophageal wave that follows a conscious
swallow
• Secondary peristalsis?
• Is the normal reflex response to a stubborn food bolus or
refluxed material designed to clear the oesophagus by a
contraction that is not preceded by a conscious swallow.
Tertiary contractions?
Are nonperistaltic waves that are infrequent (< 10%) during
laboratory based manometry, although readily detected if
manometry is undertaken while the patient eats a meal

3.
INVESTIGATION
• Plain radiographs will show?
• foreign bodies.
• Contrast radiography?(Barium swallow)
• Narrowing, space-occupying lesions,
anatomical distortion or abnormal motility.
• CT-Scan?
• The assessment of Neoplasms of the
oesophagus and perforation

4.
3.
- Diagnosis
- Clinical presentation
- Diagnosis
- Treatment

5.
• Endoscopy?
1. View the inside of the oesophagus and
the oesophagogastric junction
2. Obtain a biopsy or cytology specimen
3. Removal of foreign bodies
4. Dilate strictures

6.
• Endosonography?
• Radial; 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

7.
• 24-hour pH recording?
• The most accurate method for the
diagnosis of gastro-oesophageal reflux
An oesophageal pH < 4 at the level of the pH electrode is
conventionally considered the cut-off value and, in most oesophageal
laboratories, the total time when pH is < 4 in a 24-hour period does not
exceed 4% in a healthy adult.

8.
• perforation is more serious
• 1-Iatrogenic .
• 2-due to barotrauma’
(spontaneous perforation
• Boerhaave syndrome)
• Boerhaave syndrome is the
most serious type of
perforation because of the
large volume of material
that is released under
pressure
Perforation during diagnostic
upper endoscopy.
• Who are at increased risk?
1. Those with anterior cervical
osteophytes
2. Presence of a pharyngeal
pouch
3. Mechanical causes of
obstruction
4. Biopsy of a malignant tumor.
PERFORATION OF ESOPHAGUS
Perforation during therapeutic upper endoscopy is by?
1. Guidewires, graduated dilators or balloons
2. During the placement of self-expanding stents
3. The risk is higher in patients with malignancy.

9.
1-Defective lower
esophageal sphincter
(LES) function
2- transient LES
relaxations TLESRs)
3- hypotonic LES **
( e.g. sleroderma)
4- disruption of LES
** ( e.g. resection,
balloon rupture)
 Hiatal hernia ** ( mal
alignment of LES and
crural diaphragm)
Poor esophageal clearance
**
 Decreased salivary
protection
decreased volume ( e.g.
sicca syndrome)
 Poor gastric emptying
with
Increased intra-abdominal
pressure ( e.g. straining,
obesity, pregnancy)
 Duodenogastric reflux
GERD(GASTROESOPHAGEALREFLEX
DISORDER)

10.
Retrosternal
burning pain,
(heartburn)
 epigastric pain
regurgitation
Pulmonary
Asthma
Aspiration pneumonia
Chronic bronchitis
Pulmonary fibrosis
Other
Chest pain
Dental erosion
ENT
Hoarseness,Laryngitis,Pharyngitis
ChronicSinusitis,Subglottic stenosis
Laryngeal cancer
CLINICAL PRESENTATION

11.
 Barium swallow
 Endoscopy
 Ambulatory pH
monitoring
 Esophageal
manometry
INVESTIGATIONS

12.
GOAL OF TREATMENT
 Eliminate symptoms
 Heal esophagitis
 Manage or prevent complications
 Maintain remission

13.
LIFESTYLE MODIFICATIONS
Elevate head of bed 4-6 inches
Avoid eating within 2-3 hours of bedtime
Lose weight if overweight
Stop smoking
Modify diet
Eat more frequent but smaller meals
Avoid fatty/fried food, peppermint, chocolate,
alcohol, carbonated beverages, coffee and tea
OTC medications .

14.
H2-Receptor Antagonists
(H2RAs)
Cimetidine (Tagamet®)
Ranitidine (Zantac®)
Famotidine (Pepcid®)
Nizatidine (Axid®)
Proton Pump Inhibitors
(PPIs)
Omeprazole (Prilosec®)
Lansoprazole (Prevacid®)
Rabeprazole (Aciphex®)
Pantoprazole (Protonix®)
Esomeprazole (Nexium ®)
ACID SUPPRESSION THERAPY FOR
GERD

15.
BARRETT’S ESOPHAGUS; DEFINITION
• defined short segment (3 cm or low) orlong
segment (more than 3 cm) barrett’s esophagous.
• The present definition requires both endoscopic recognition of
colummar lining and biopsy-established intesttinal metapolism in the
esophagous.
• the tube that carries food from the mouth to the stomach -- changes to tissue
that resembles the lining of the intestine. About 10% of people with chronic
symptoms of GERD develop Barrett's esophagus.

16.
Etiology
1. GERD → esophageal acid exposure and bile
exposure → Barrett’s esophagus → esophageal
Adenocarcinoma
2. Chronic GERD is the mian risk factors developing
Barrett’s esophagus
3. Obesity
4. Cigarette smoking and a high-fat diet
5. Genetic component

17.
BARRETT’S ESOPHAGUS
Complications of Barrett’s esophagus :
(1)ulcer
(2)stricture
(3)dysplasia
(4)cancer
Endoscopy land & biopsy technique;
• Four-quadrant biopsies should be obtained at
2 cm intervals through the columnar-lined
esophagus from distal to proximal.
• Detection Barrett’s length.

18.
Another pathologist ←
Repeated biopsy ←
Intestinal metaplasia
without dysplasia
Low grade
dysplasia
Repeated
Biopsy
High grade
dysplasia
Barrett’s esophagus
Medical
treatment
Two biopsy (3 years)
One biopsy per year
High grade
dysplasia +Cancer ?
Positive
Negative
Careful survillance ←
Endoscopic ablation
therapy ←
Esophagectomy ←
Esophagectomy ←

19.
TREATMENT
• Barrett’s esophagus without high grade dysplasia
or cancer
(A): First medical treatment:
→ (proton pump inhibtor better than H2 blocker)
→ 95% with errosive gastritis and barrett’s ulcer
healed.
→ decrease DGE (bile) reflux (decrease secretion).
→ medical therapy can’t regress Barrett’s EP but
improved symptoms.

20.
SURGICAL TREATMENT
• Anti reflux surgery can’t regress Barrett’s EP
and complete prevention of Adeno carcinoma.
Indication for surgery:
1. Transmural penetrated ulcer
2. Severe stricture
3. Perforated ulcer
4. High grade dysplasia & cancer.
5. Massive & uncontroled bleeding from ulcer
6. Fistula fo rmation
24

21.
CARCINOMA OF THE OESOPHAGUS
• Risk factor
• - SCC:
• smoking and alcohol consumption,
• dietary (N-nitroso compounds, hot food, betel nut, poor nutrition), HPV infection,
Endemic areas (China)
• - adeno:
• smoking, obesity, GERD, long term use of theophylline, and beta agonists )
?
(
25

22.
WHAT ARE THE CLINICAL FEATURES OF CA
ESOPHAGOUS?
1. Early disease; non-specific dyspeptic symptoms
2. Dysphagia, regurgitation, vomiting, odynophagia
3. Weight loss
4. Chronic GI blood loss is common & may result in iron deficiency anemia.
• Acute bleeding is rare. (erosion to aorta or pulmonary arteries.)

23.
WHAT ARE THE CLINICAL FEATURES OF CA
ESOPHAGOUS?
1. Advanced malignancy include recurrent
laryngeal nerve palsy, Horner’s syndrome,
chronic spinal pain and diaphragmatic
paralysis.
2. Cutaneous tumour metastases or
enlargedsupraclavicular lymph nodes
3. Respiratory symptoms can be caused by
aspiration and direct invasion of the
tracheobronchial tree.

24.
DIFFERENTIAL DIAGNOSIS OF DYSPHAGIA
1. Esophageal carcinoma
2. Achalasia
3. Peptic strictures due to reflux
4. Benign esophageal tumors
(rare)

25.
6.
Diagnosis

26.
ACHALASIA

27.
COMPLICATIONS OF GE REFLUX
ESOPHAGITIS PEPTIC STRICTURE

28.
EsophagealCancer

29.
Squamous cell
carcinoma of
Esophagus -
“Esophagus:
contrasted barium
shows squamous cell
carcinoma in the
middle portion of

30.
Figure 1. Initial CT scan revealed
a large mass in the distal third
of the esophagus.
Post-chemotherapy CT scan
showed a significant reduction of
the tumor size.

31.
Carcinoma esophagus- a barium swallow showing
irregular narrowing with "shouldered edges" suggestive
of a malignant stricture!!

32.
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