ESOPHAGUS

Anatomy
The esophagus is a muscular tube about
ten inches (25 cm.) long, extending from
the hypopharynx to the stomach.
The esophagus lies posterior to the trachea
and the heart and passes through the
mediastinum and the hiatus, an opening in
the diaphragm, in its descent from the
thoracic to the abdominal cavity.
The esophagus has no serosal layer; tissue
around the esophagus is called adventitia.

Cervical
Cervical begins at the lower end of
pharynx (level of 6th vertebra or
lower border of cricoid cartilage) and
extends to the thoracic inlet
(suprasternal notch); 18 cm from
incisors.

Thoracic
Upper thoracic: from thoracic inlet to level
of tracheal bifurcation; 18-23 cm.
Mid thoracic: from tracheal bifuraction
midway to gastroesophageal junction; 2432 cm.
Lower thoracic: from midway between
tracheal bifurcation and gastroesophageal
junction to GE junction, including
abdominal esophagus; 32-40 cm.

Abdominal
Considered part of lower thoracic
esophagus; 32-40 cm.

Anatomy
The esophagus
has three distinct
areas of naturally
occurring
anatomic
narrowing
Cervical
constriction
Bronchoaortic
constriction
Diaphragmatic
constriction

Esofagus

1.
2.
3.
4.

Esophagus Atresia
Corrosive Esophagus
Esophagitis
Gastro Esophageal reflux

1. Esophageal Atresia
Defenisi

EASOPHAGEAL ATRESIA It is the

failure of the esophagus to form
a continuous passage from
pharynx to stomach during
embryonic
development
resulting in obstruction in infants
normal swallowing routes.

 Etiologi
-Unknown Chromosomal anomalies
(trisomy 18, trisomy 21, and trisomy 13)
-Failure of embryonic development
Digestive tract problems(diaphragmatic
hernia, intestinal atresia or
imperforated anus .)
-Congenital heart diseases

PATHOPHYSIOLOGY
- Esophagus developed from first segment of

embryonic gut.During the 4 th and 5 th week of

gestation , forgut normally lengthens and separate
longitudinally and longitudinal portion fuse to form
parallel channels .
- Anomalies involving trachea and esophagus are
caused by defective incomplete fusion of the
tracheal folds following separation or altered cellular
growth during embryonic development.

Classification

Esophageal Atresia

1 per 2500 3500 live births

Sporadic, non-syndromal

Dysmotile distal esophagus

Deficiency of tracheal cartilage

50% have 1 or more associated

anomalies: cardiac, anorectal, GU,
vertebral/skeletal, others

2. Corrosive Oesophagitis
DESCRIPTION
Esophageal stricture is narrowing of
the esophagus (the tube connecting
the mouth to the stomach) caused by
inflammation. The narrowing
interferes with swallowing.
Corrosive esophagitis is narrowing of
the esophagus caused by chemical
damage.

FREQUENT SIGNS AND SYMPTOMS

Sudden or gradual decrease in the ability to
swallow. Gradual swallowing difficulty affects
solid foods first, then liquids.
Pain in the mouth and chest after eating.
Increased salivation.
Rapid breathing.
Vomiting, sometimes with mucus or blood.
Cancer of the esophagus often causes
similar symptoms.

Diagnosis
Laboratory
radiologi

Esofagitis korosif, after 3 week

Esofagitis korosif, after 5

moon

CAUSES
Scarring of the esophagus following inflammation or
damage caused by:
Chronic heartburn (reflux esophagitis) or hiatal hernia.
Prolonged use of feeding tubes.
Accidental swallowing of lye or other corrosive
chemicals by a child. This is an emergency!
Deliberate swallowing of lye or other corrosive
chemicals by a suicidal person.
Bulimia.
Radiation therapy to throat, neck or chest.

RISK INCREASES WITH

Careless storage of corrosive
chemicals, such as lye,
kerosene, harsh detergent or bleach.
PREVENTIVE MEASURES
Store all chemicals out of the reach
of young children.
Avoid prolonged use of feeding
tubes.

TREATMENT
GENERAL MEASURES
Diagnostic procedures such as endoscopy (an
endoscope[an optical instrument with a lighted tip] is
inserted into the esophagus, which allows visual
examination of the cavity). A small amount of tissue will
be removed for biopsy to make sure the stricture is
benign. Also Xrays of the esophagus (barium swallow)
may be recommended.
The stricture must be stretched regularly (about once a
month) with large, heavy dilators. The stricture will
eventually return if regular treatments are not continued.
Surgery to remove stricture if other measures fail (rare).

3.Reflux Oesophagitis
Esophagitis is an inflammation of the lining
of the esophagus, the tube that carries
food from the throat to the stomach.
If left untreated, this condition can become
very uncomfortable, causing problems with
swallowing, ulcers, and scarring of the
esophagus. In some instances, a condition
known
as
Barrett's esophagus
may
develop, which is a risk factor for
esophageal cancer.

Oesophagitis
Grading
Savary-Millar
0 Normal
1 Isolated erosion, Streak, Erythema
2 >1 erosion, non confluent
3 Confluent / circumferential without
stenosis
4 Ulceration, Stricture, Barretts

 Los Angeles
A 1 mucosal breaks 5mm
B 1mucosal breaks >5mm
C mucosal breaks extending over 2
mucosal folds, <75% circumference
D Mucosal breask involving > 75%
circumference

Esophagitis is caused by an infection

or irritation in the esophagus. An
infection can be caused by bacteria,
viruses, fungi, or diseases that
weaken the immune system.
Infections that cause esophagitis
include:
Candida
Herpes

Symptoms of esophagitis include:

Difficult and/or painful swallowing
Heartburn
Mouth sores
A feeling of something of being stuck
in the throat
Nausea
Vomiting

 Thorough physical examination and

reviewed your medical history, there
are several tests that can be used to
diagnose esophagitis. These include:
Upper endoscopy .
Biopsy.
Upper
GI series (or barium swallow)

Treatment :
Medications that block acid production such as
heartburn drugs.
Antibiotics, anti-fungals, or antivirals to treat an
infection.
Pain
Corticosteroid
Intravenous (by vein) nutrition to allow the esophagus
to heal and to prevent dehydration and malnutrition.
Endoscopy
Surgery to remove the damaged part of the esophagus.

Complications
Bleeding
Stricture
Barretts

4.Gastroesophageal Reflux
Disease
1/3 Western population experience
symptoms at least once a month
4-7% daily
Most patients with mild symptoms
carry out self-medication
The prevalence and severity of GERD
is increasing

Typical GERD Symptoms

Heartburn
substernal burning or chest pain
worse with spicy foods, tomato
sauce, citrus juices, chocolate,
coffee, and alcohol
1 to 2 hours after eating, often at
night, relieved by antacids and OTC
H2 blockers
Regurgitation
sensation that fluid or food is
returning into the esophagus

 Dysphagia
up to 40% of pts with GERD have
sensation of food hanging up in the
lower esophagus--esophageal
dysphagia
typically limited to only solid food,
with normal passage of liquids,
suggesting mechanical disorder
develops slowly enough that the
patient may adjust eating habits
unknowingly

Atypical GERD Symptoms

Cough, asthma, hoarseness, and
noncardiac chest pain
primary complaint in 20-25%
more difficult to prove a cause-andeffect relationship
trial of high-dose PPIs is helpful
make sure patient doesnt have
another cause for pain

Pathophysiology of GERD

Fundic distention because of overeating

LES is taken up by the expanding fundus,
exposing the squamous epithelium/LES to
gastric juice
Worsened by delayed gastric emptying with high-fat diet
and hiatal hernia

Compensated with increased swallowing

Saliva bathe the injured mucosa and alleviate the
discomfort
= aerophagia, bloating, repetitive belching
More distension leads to further exposure and
repetitive injury to the terminal squamous
epithelium leading to inflammation

continued epigastic pain and possibly epithelial

columnarization

Extension of the inflammatory process into

Gastroesopha
geal Reflux

Diagnosis of GERD

Based on symptoms alone?

Correct in only 2/3 of patients
these symptoms are not specific for GE
reflux

achalasia, diffuse spasm, esophageal

carcinoma, pyloric stenosis, cholelithiasis,
gastritis, gastric or duodenal ulcer, and
coronary artery disease

need objective diagnosis before

the decision is made for surgical
treatment

Diagnosis of GERD

First episode
Initial therapy with H2 blockers or PPI for 12 weeks

Failure of H2 blockers or PPI to control the symptoms suggests

that either the diagnosis is incorrect or the patient has severe
disease
EGD
Opportunity for assessing the severity of mucosal damage
24-hour pH and bilirubin monitoring
Measurement degree and pattern of esophageal exposure to
gastric and duodenal juice
Manometry
Assess the status and function of the LES and esophageal body

These studies identify features that predict a poor response to

medical therapy, frequent relapses, and the development of
complications

Complications of GERD
Mucosal complicationsesophagitis and stricture
Extraesophageal or Respiratory
complications, such
as laryngitis,
recurrent pneumonia, and
progressive pulmonary fibrosis
Reflux (aspiration) vs reflex
(vagal bronchoconstriction)
Metaplastic and Neoplastic
complications, Barrett's and
esophageal adenocarcinoma

Summary of Pathogenesis of GERD

impaired lower esophageal
sphincter-low pressures or frequent
transient lower esophageal sphincter
relaxation
2, hypersecretion of acid
3, decreased acid clearance resulting
from impaired peristalsis or abnormal
saliva production
4, delayed gastric emptying or
duodenogastric reflux of bile
salts and pancreatic enzymes.
1,