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Prof.

Mutti Ullah Khan


Medical Unit III
Services Hospital
Anatomy of Esophagus
Hollow tube formed of striated muscle (upper
part) and smooth muscle (lower part).
Length about 20-30 cm in adults.
Fibers of the cricopharyngeus muscle
represent the upper esophageal sphincter
(UES).
In thoracic cavity it lies in posterior
mediastinum, posterior to the trachea.
Leaves thorax through diaphragmatic hiatus
Lower esophageal sphincter (LES) about 3-5
cm long, ?physiological sphincter.
Microscopic Anatomy of esophagus
Mucosa:
Lined with stratified squamous epithelium, rich
in glycogen.
Lamina propria
muscularis mucosa : thin layer of smooth
muscle
Submucosa
The outer muscular layers: striated in the
upper part and smooth in lower 2/3
No serosal covering.
Physiology
UES: tonically closed, opens 0.2-0.3 sec
after a swallow.
Peristaltic contractions, duration less than
7 sec and amplitude less than 150 mmHg,
velocity less than 8 cm/sec
LES: tonically closed at rest, pressure 20
mmHg, cholinergic mediated, relaxes with
swallowing.
Transient LES relaxation, independent of
swallowing is the major cause of reflux.
Motor disorders of the esophagus
Achalasia
Localized esophageal spasm
Diffuse esophageal spasm
Nutcracker esophagus
Non-specific motor abnormalities
Achalasia
Failure of relaxation of the LES
with swallowing and aperistalsis
in lower esophagus.
Due to decreased or absent
intramural esophageal ganglion
cells.
Symptoms of Achalasia
Dysphagia to fluids and solids, intermittent, long
-standing.
Regurgitation of undigested food
Chest pain
Aspiration
Weight loss
Diagnosis of achalasia
Esophageal manometry:
Absent peristalsis
High LES pressure
Failure of relaxation of LES.
Radiographic studies
Endoscopy to exclude organic disease.
Normal Achalasia
TREATMENT OF ACHALASIA
Management Goals
Relieve symptoms
Improve esophageal emptying
Prevent development of megaesophagus
TREATMENT OF ACHALASIA
 Drug therapy
 Smooth muscle relaxants
 Botulinum toxin injection
 1 to 2 years relief
 Symptomatic relief
 Semisoft bland diet
 Eating slowly
 Drinking with meals
 Sleeping with Head end elevated
Endoscopic pneumatic dilation
 Outpatient procedure
 LES disrupted using balloons of progressively larger diameters
 Repeat dilations are often required
Surgical myotomy
DEFINITIONS
Gasrtoesophageal reflux: Reflux of gastric
contents to the esophagus
Gastroesophageal reflux disease (GERD): Any
significant symptomatic clinical condition or
histopathological changes resulting from
reflux.
Reflux esophagitis: GERD patients with
histopathologically demonstrable changes in
the esophageal mucosa.
Epidemiology of GERD
Heartburn is a very common condition:
3% of population experience heartburn daily
7% frequently
15% weekly
25% monthly
Most common in pregnant women: 80%
Common in obese and smokers
Mechanisms of GERD
Transient LES relaxation
Hypotensive LES
Decreased esophageal acid clearance
Hiatus hernia
Impaired salivation.
CLINICAL PICTURE OF GERD
ESOPHAGEAL SYMPTOMS
EXTRAESOPHAGEAL SYMPTOMS
ESOPHAGEAL SYMPTOMS OF
GERD
HEARTBURN
REGURGITATION
Bad Breath
Dysphagia
Chest pain
Water brash
Nausea and vomiting
Belching
Hiccup
EXTRAESOPHAGEAL SYMPTOMS OF
GERD
Chronic cough
Asthma
recurrent pneumonitis
nocturnal choking
hoarseness of voice
posterior laryngitis with ulceration and
granuloma formation.
sore throat
dental disease
Earache
Globus sensation
Diagnosis of GERD
Clinical picture.
UGI endoscopy.
24 hour pH monitoring
Radioisotope scanning
Barium swallow.
Complications of GERD
Stricture formation
Chronic blood loss
Barrett’s epithelium
Narrow band imaging & chromoendoscopy with
methylene blue are used as diagnostic tool.
Adenocarcinoma
Savary Gillard dilator used for
dilatation of esophageal strictures
Barrett’s epithelium
Barrett’s epithelium
 Narrow Band Imaging used for diagnosis of barrett’s epthelium
Barrett’s epithelium
 Chromoendoscopy using methylene blue used for diagnosis of Barrett’s
Natural history of GERD
May be acute condition in a small percentage
Mostly chronic condition with recurrent
symptoms
Majority can be controlled on drugs
Majority may require a sort of acid
suppressive therapy at 5 years
No clear relation exists between symptoms of
reflux, amount of reflux or degree of
esophagitis.
Management of GERD
Life- style modification:
 avoid cigarette smoking
 dietary manipulation: decrease fatty, spicy and
acidic foods
 decrease weight
 elevation of the head of the bed
 avoid tight abdominal binders
 avoid constipation
 avoid large meals
 avoid drugs which decrease LES pressure
 avoid sleeping after meals for at least 3 hours.
Pharmacologic therapy of GERD
Antacids:
 Mg trisilicate
 Aluminium hydroxide
Ca carbonate
sodium bicarbonate.
H2-blockers:
 Cimetidine
ranitidine
famotidine
nizatidine
Pharmacologic therapy of GERD
Proton pump inhibitors:
 Omeprazole
lansoprazole
pantoprazole
rabeprazole
Esomeprazole
Tenatoprazole
Prokinetic drugs:
metoclopramide
domperidone.
Endoscopic therapy for GERD
Sterrata procedure
Entyrex
Gate keeper anti-reflux repair
Gastric plication
Antireflux

surgery
Indications:
complicated reflux
non compliance for medication
refractory GERD
patient’s preference
severe disease in young person
Most popular operation now is
laparoscopic fundoplication
Treatment of Barrett’s epithelium
BE usually occurs in longstanding severe
reflux disease
BE does not regress after fundoplication or
PPI therapy
Screening for dysplasia?
If high grade dysplasia found:
esophagectomy
Ablation of BE:
Photodynamic therapy
Argon plasma coagulation
Endoscopic mucosal resection

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