Barrett’s, Stricture, Cancer, HHO,

Dr. H. Rustam Effendi YS,SpPD-KGEH

Divisi Gastroenterologi dan Hepatologi
Departemen Ilmu Penyakit Dalam FKUSU/
RSUP H. Adam Malik - RSU Dr. Pirngadi Medan

15 Oktober 2012
 Definition
• Normal distal esophagus — may display short
cephalad extention of columnar epithelium
above the gastroesophageal junction.
• An endoscopic diagnosis.
• Circumferential, columnar epithelial lining of
distal esophagus extending at least 3 cm
above the gastroesophageal junction.
 Prevalence
• 2% of patient undergoing panendoscopy.
• 44 % patient of peptic stricture with Barrett’s
esophagus.
• 27/100000.
• Autopsy 376/100000.
• Most barrett’s esophagus are asymptomatic.
 Clinical feature
• Asymptomatic.
• GER and complication.
• Heartburn, regurgitation.
• Dysphagia from stricture or carcinoma.
• Tobacco and alcohol use.
 Radiology
• Difficult to diagnose by radiography.
• Sliding hiatal hernia with esophagitis.
 Endoscopy
• Essential to confirm diagnosis.
• Squamous epithelium is more smooth, pale, the
columnar epithelium is more granular, reddish. and
often contain signs of reflux injury.
• Endoscopic biopsy should be performed in all
suspected cases, to confirm the search for dysplasia.
• Methylene blue associated stain area of epithelial
dysplasia to guide biopsies.
 Ulceration and stricture
• More in patient with Barrett’s esophagus（10-15%）
than in GER.
• Ulcer penetrate the columnar epithelium, like the
gastric ulcer, acid-peptic erosion, alkaline reflux.
• s/s — bleeding, pain, obstruction（30%）,
perforation, irondeficiency anemia, dysphagia,
perforation into pleural space, lung, pericardium.
• Stricture always at squamocolumnar junction.
 Dysplasia
• Low and high grade.
• Loss pf nuclear polarity, hyperchromatism,
nuclear enlargement, stratification,
pleomorphism, abnormal mitoses.
• Distinguish high and low grade is difficult.
 Adenocarcinoma
• Distinguish adenocarcinomna in Barrett’s
esophagus from carcinoma of cardia is difficult.
• 30-125 times the risk of normal population.
• 1 case per 100 patient-year, annual risk 1%.
 Benign Barrett’s esophagus
• Asymptomatic and uncomplication not require
treatment.
• Medical treatment of GER infrequently regression
the Barrett’s epithelium, or only partial, island or
underlying columnar epithelium, still at risk for
dysplasia.
• Treatment use the same guideline for GER.
• Antireflux surgery not lessen risk of malignant
degeneration of Barrett’s epithelium.
 Stricture
• Periodic dilation, weight loss, elevated head of
bed, dietary modification.
• Transabdominal Nissen fundoplication
coupled with intraoperative dilation.
• Left thoracotomy for complete esophageal
mobilization to permit lengthening procedure
as Collis’ gastroplasty if any display evidence
of esophageal shortening.
 Patogenesis Striktur Esofagus

Peptic esofageal sricture Komplikasi jangka panjang dari

GERD.
Sekitar 40-65% kasus GERD akan berkembang menjadi
esofagitis erosi dan bila tidak diobati sekitar 4-23% esofagitis
erosi ini akan berkembang menjadi striktur esofagus.
• Faktor predisposisi 1.Refluks yang lama,
2.adanya kelainan motilitas esofagus dan
3.tekanan spingter bawah esofagus yang rendah
• Caustic esophageal stricture Tertelannya zat korosif .Luas dan
beratnya kerusakan tergantung pada jenis zatnya, jumlah,
konsentrasi, bentuk fisik zat dan lamanya kontak
• Striktur >> Tempat persilangan esofagus dengan bronkus
utama kiri dan pada bagian bawah esofagus
 Striktur Esofagus
• Striktur Terjadi dalam 6 minggu sampai 10
bulan setelah tertelan zat korosif.
• Striktur esophagus maligna Paling sering
terjadi di bagian distal, tengah dan proksimal.
• Keganasan esofagus ini dapat berasal dari
lapisan mukosa, submukosa atau bisa juga
disebabkan oleh metastase keganasan di luar
esofagus.
• Keganasan mukosa paling sering berupa
karsinoma sel skuamosa dan hanya sebagian
kecil adenokarsinoma. Metastase keganasan di
luar esofagus dapat berasal dari paru, payudara
dan ovarium.
 Barrett’s ulcer
• Most heal with medical therapy —, PPI,
prolong therapy exceeding 8 weeks, response
rate 85%.
• Recurrence common.
• If ulcer fail to heal after medical treatment 4
months, the antireflux surgery — Collis’-Belsey
repair, Collis’-Nissen fundoplication.
 Low-grade dysplasia
• Early signal that carcinoma may develop.
• Most low grade not progress to high grade or
invasive carcinoma.
• Medical therapy is recommended even in
absence of symptoms.
• More frequent endoscopic surveillance to
ensure prompt detection.
 High-grade dysplasia

• Indication of esophagectomy.
• 22-73% chance unsuspected invasive
carcinoma.
• Esophagogastrectomy.
• 100% cure rate patient without invasive
tumor.
• Thermal laser, photodynamic therapy —
long term efficacy and cost-effectiveness
unknown.
 Adenocarcinoma
• Esophagogastrectomy.
• Higher respectability — 94-100%.
• Long term survival similar — 20% in 5-year.
 BARRETT’S ESOPHAGUS

• The normal tan upper BARRETT’S

esophageal mucosa is at
the far left
• The distal esophagus -
Barrett mucosa (columnar
metaplasia)
• a large ulcerating
adenocarcinoma that
extends into stomach
(Adenocarcinomas can
normal
arise in Barrett esophagus)
 BARRETT’S ESOPHAGUS

• Gastric-type mucosa above the

gastroesophageal junction
• The metaplasia results from
chronic gastroesophageal reflux
disease (GERD
• Columnar epithelium to the left
and the squamous epithelium at
the right
• “Typical" Barrett's mucosa,
because there is intestinal
metaplasia as well (note the
goblet cells in the columnar
mucosa).
• Esophagus
Tumors
• 1. Leiomyoma
– MC benign tumor of esophagus arising from Smooth muscle
cells
• 2. Squamous cell carcinoma
– Incidence: common in China, Rare in US (Adenocarcinoma –
MC in USA) M>F, age >50 yr.
– Risk factors : cigarette smoking, alcohol, nitrosamines in the
preserved foods, fungus contaminated foods
– 50%are in middle 1/3rd
– “Early carcinoma” = upto submucosa ( 90%- 5 year survival
good prognoses even though lymph nodes are involved)
– Spreads locally into mediastinal structures & to lymph nodes
– Clinically:
• Insidious dysphagia, weight loss, hemorrhage, Esophago -
tracheal fistula.
• Overall 5-year-survival is 5%.
• Esophagus
Tumors
• 3. Esophageal adenocarcinoma
• Incidence: <25% of esophageal cancers world wide
• up to half of all esophageal cancers reported in US
• Primary risk factor - Barrett’s esophagus
• Most arise in distal 1/3rd of the esophagus.
• Histology: Mucin producing tubular (intestinal), or signet cell/ring
(gastric/infiltrative) carcinoma, undifferentiated.
• present with dysphagia
• Overall 5-year survival - 15%
 Esophagus
Squamous cell carcinoma

• irregular reddish,
ulcerated exophytic
most common in
mid-esophageal
mass as seen on the
mucosal surface
(squamous cell
carcinoma)
 Esophagus
Squamous cell carcinoma
• neoplastic cells have
abundant pink cytoplasm
and distinct cell borders
typical for squamous cell
carcinoma
• Esophageal carcinomas
are not usually detected
early and, therefore,
have a very poor
prognosis
• in the lymphatics
 Esophagus
Malignant Tumors

Feature Squamous Adeno

Incidence 75% 25%
Geography Asia USA
Age >50 >40
Site Middle1/3 rd Lower 1/3rd
Risk factors Smoking, Reflux Esophagitis
alcohol, foods (Barrett's)
Prognosis 5yr.-5% 5yr.-15%
1.1
2.1
2.2
 Esophageal Cancer
• Malignant neoplasm of esophagus
• 14,520 new cases of esophageal cancer
annually
• 13,570 deaths annually
• 5-year survival rate <20%
 Esophageal Cancer
• Adenocarcinomas
– Arise from glands lining esophagus
– Resemble cancers of stomach and small intestine
– 30% to 70% of esophageal cancers
– Incidence in distal esophagus currently ↑
• Squamous cell
– Incidence currently ↓ in United States
 Esophageal Cancer
Etiology and Pathophysiology
• Cause is unknown
• Incidence ↑ with age
• ↑ Incidence in African Americans and Alaska
Natives
 Esophageal Cancer
Etiology and Pathophysiology
• Risk factors
– Smoking
– Excessive alcohol intake
– Barrett’s esophagus
– Diets low in fruits and vegetables
 Esophageal Cancer
Etiology and Pathophysiology
• Risk factors (cont’d)
– Certain minerals and vitamins
– Exposure to lye, asbestos, and metal
– History of achalasia
 Esophageal Cancer
Etiology and Pathophysiology
• Majority of tumors located in middle and
lower portion of esophagus
• Malignant tumor
– Usually appears as ulcerated lesion
– May penetrate muscular layer and outside wall of
esophagus
– Obstruction in later stages
 Esophageal Cancer
Clinical Manifestations
• Symptom onset is late
• Progressive dysphagia is most common
– Initially with meat, then soft foods and liquids
• Pain develops late
– Substernal, epigastric, or back areas
• Increases with swallowing
• May radiate
 Esophageal Cancer
Clinical Manifestations
• Weight loss
• Regurgitation of blood-flecked esophageal
contents
 Esophageal Cancer
Clinical Manifestations
• If tumor is in upper third of esophagus
– Sore throat
– Choking
– Hoarseness
 Esophageal Cancer
Complications
• Hemorrhage
– If erodes into aorta
• Esophageal perforation with fistula formation
• Esophageal obstruction
• Metastasis
– Liver and lung common
 Esophageal Cancer
Diagnostic Studies
• Endoscopy with biopsy
– Necessary for definitive diagnosis
• Endoscopic ultrasonography (EUS)
– Important tool to stage
• Barium swallow with fluoroscopy
 Esophageal Cancer
Diagnostic Studies
• Bronchoscopic examination
– Detect involvement of lung
• Computed tomography (CT)
• Magnetic resonance imaging (MRI)
 Esophageal Cancer
Collaborative Care
• Treatment depends on location and spread
• Poor prognosis
– Usually not diagnosed until advanced
• Best results with combination therapy
 Esophageal Cancer
Collaborative Care
• Photodynamic and/or laser therapy
– Used to ablate mucosal adenocarcinoma or
Barrett’s
– Porfimer (Photofrin): Photosensitizer
• Injected IV
• Absorbed by most tissue
• Selectively kept to a greater degree by neoplastic tissue
 Esophageal Cancer
Collaborative Care
– Porfimer (cont’d)
• Light transmitted through endoscope
• Must avoid direct sunlight up to 4 weeks after
• Endoscopic mucosal resection (EMR)
– Removes superficial lesions
– Submucosal neoplasms
 Esophageal Cancer
Collaborative Care
• Surgical procedures
– Esophagectomy
• Removal of part or all of the esophagus
• Use of Dacron graft to replace resected part
– Esophagogastrostomy
• Resection of a portion of esophagus and anastomosis
of remaining portion to stomach
 Esophageal Cancer
Collaborative Care
• Surgical procedures (cont’d)
– Esophagoenterostomy
• Resection of a portion of esophagus and anastomosis
of segment of colon to remaining portion
• May be open or laparoscopic
 Esophageal Cancer
Collaborative Care
• Concurrent radiation and chemotherapy
– Slows progression
– Sometimes started before surgery
 Hiatal Hernia
• Herniation of portion of the stomach into
esophagus through an opening or hiatus in
diaphragm
• Also referred to as diaphragmatic hernia and
esophageal hernia
• Most common abnormality found of x-ray of
upper GI
• More common in older adults and in women
 Hiatal Hernia
• Two types
– 1. Sliding
• Stomach slides into thoracic cavity when supine, goes
back into abdominal cavity when standing upright
• Most common type
– 2. Paraesophageal or rolling
• Esophageal junction remains in place, but fundus and
greater curvature of stomach roll up through
diaphragm
Hiatal Hernia

Fig. 42-7
 Hiatal Hernia
Etiology and Pathophysiology
• Cause is unknown
• Many factors involved
– Structural changes
• Weakening of muscles in diaphragm
– Increased intraabdominal pressure
• Obesity
• Pregnancy
• Heavy lifting
 Hiatal Hernia
Etiology and Pathophysiology
• Factors (cont’d)
– Increasing age
– Trauma
– Poor nutrition
– Forced recumbent position
– Congenital weakness
 Hiatal Hernia
Clinical Manifestations
• May be asymptomatic
• Symptoms include
– Heartburn
• After meal or lying supine
– Dysphagia
 Hiatal Hernia
Complications
• GERD
• Esophagitis
• Hemorrhage from erosion
• Stenosis
• Ulcerations of herniated portion
• Strangulation of hernia
 Hiatal Hernia
Complications
• Ulcerations of herniated portion
• Strangulation of hernia
• Regurgitation with tracheal aspiration
• Increased risk of respiratory problems
 Hiatal Hernia
Diagnostic Studies
• Barium swallow
– May show protrusion of gastric mucosa through
esophageal hiatus
• Endoscopy
– Visualize lower esophagus
– Information on degree of inflammation or other
problems
 Hiatal Hernia
Conservative Therapy
• Lifestyle modifications
– Eliminate alcohol
– Elevate HOB
– Stop smoking
– Avoiding lifting/straining
– Weight reduction, if appropriate
 Hiatal Hernia
Surgical Therapy
• Reduction of herniated stomach into
abdomen
• Herniotomy
– Excision of hernia sac
• Herniorrhaphy
– Closure of hiatal defect
 Hiatal Hernia
Surgical Therapy
• Antireflux procedure
• Gastropexy
– Attachment of stomach subdiaphragmatically to
prevent reherniation
 Hiatal Hernia
Surgical Therapy
• Goals
– Reduce hernia
– Provide acceptable lower esophageal sphincter
(LES) pressure
– Prevent movement of gastroesophageal junction
Nissen Fundoplication

Fig. 42-5
• Esophagus
• Structures :
– UES (upper esophageal sphincter) –
• made up of skeletal muscle Cricopharyngeus muscle
• Involved in scleroderma or systemic sclerosis
– LES (lower esophageal sphincter) opens into the stomach
• gastro-esophageal junction ( 3 cm ), if >3cm is called as ?
• transitional zone which is columnar
• 1.Congenital anomalies : produce choking on breast feeding
• Atresia (noncanalized segment)
• Fistulas (Connection/opening between esophagus and trachea)
– several types
• Webs (produce dysphagia to solids)
– Webs - Plummer-Vinson / Paterson-Kelly syndrome( post
cricoid web, IDA, Glossitis, cheilosis in perimenopausal female,
Risk of postcricoid Squamous cell carcinoma )
• Schatzki’s rings
– At LES
– Cause narrowing (Stenosis)
• Stenosis
– MCC: Gastro-esophageal reflux
– Most commonly acquired (corrosives, radiation, Scleroderma
CREST syndrome)
– Major symptom - Dysphagia
• 2. Lesions with motor dysfunction
• A) Achalasia cardia ("failure to relax." )
– Affect adults
– 1) Aperistalsis
– 2) Complete or partial relaxation of LES with swallowing
– 3) Increased resting tone of LES
• 2. Lesions with motor dysfunction
• A) Achalasia cardia ("failure to relax." )
• Complications
– Aspiration pneumonia
– Candidal esophagitis ( due to stagnation of food)
– Diverticulae
– squamous cell carcinoma (2 to 5 % of affected)
• Also Caused by
1. Chaga’s disease (Trypanosoma cruzi)
2. Diabetic autonomic neuropathy
• B) Hiatal Hernia
– Upward protrusion of part of stomach through the diaphragmatic
esophageal foramen
• 2. Lesions with motor dysfunction
• B) Hiatal Hernia
– Upward protrusion of part of stomach through the diaphragmatic esophageal
foramen
• C) Diverticula (True)
– Out-pouching of the esophageal wall (contains all visceral layers) Z
– false Diverticulae – out-pouching of mucosa and submucosa only
• A) Zenker’s (pharyngeal) diverticulum T
– Seen as mass in neck of elderly pt. above UES
– Due to disordered cricopharyngeal motor dysfunction
– Produce Food regurgitation & dysphagia E
– B) Traction Diverticulum:
– Asymptomatic & Located near midpoint of esophagus
• C) Epiphrenic Diverticulum:
– Located just above the LES
– Caused by Dys -coordinated peristalsis and motor dysfunction of LES.
– cause regurgitation of food and aspiration pneumonia
 Hiatal Hernia

Sliding Rolling
•(>90%) •(para-esophageal)
• Shortened esophagus hernia(<10%)
•Dragging part of the •Part of the stomach
stomach into the thoracic (fundus) herniates
cavity alongside esophagus into
•(stomach continuous with the thorax
esophagus) •Vulnerable to serious
strangulation

prone to ulceration, bleeding, dysphasia.

• 3. lacerations
• Mallory- Weiss Syndrome
– at the gastro-esophageal junction (GEJ)
– Caused by: excessive vomiting in presence of spasm of LES
– Most common in alcoholics & Pregnancy
– Irregular longitudinal tear in the GEJ involve only the mucosa
– Boerhaave’ syndrome -tear penetrates all layers of esophagus
– Clinically Mallory-Weiss cause severe hematemesis = vomiting of
blood ( Boerhaave’s produce mediastinitis or peritonitis)
• 4. Esophageal Varices
– dilated tortuous submucosal veins
– Seen in long-standing cirrhosis with portal HTN
– 50% of cirrhotics bleed & die of Varices (MCC of death)
• 4. Esophagitis
• Causes:
• 1) Reflux of gastric contents (reflux esophagitis)
– MCC of esophagitis
– distal part of esophagus is affected
– Clinically : Dysphagia, heartburn, regurgitation, develop Barrett’s
esophagus in Long standing cases
• 2) Barrett’s Esophagus
– A complication of long-standing gastroesophageal reflux
– Columnar metaplasia of the distal esophagus
– 30 times more risk of cancer (Adenocarcinoma) in lower
esophagus