Departemen Bedah

Fakultas Kedokteran USU

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; 24-32 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. Esophagus Atresia
2. Corrosive Esophagus
3. Esophagitis
4. 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
worse at night or when lying down after a
meal

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-and-effect
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
the muscularis propria
leading to a permanently defective sphincter


Gastroesophageal
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 complications-esophagitis 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
1, 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.
Thank You