Transcript BARRETT’S ESOPHAGUS

BARRETT’S ESOPHAGUS
GENERAL THORACIC SURGERY
CHAPTER 141
HISTORY
• Norman Barrett(1950) — congenitally short
esophagus with an intrathoracic stomach.
• Allison and Johnstone (1953) and LortatJacob (1957)—an abnormal columnar
epithelium lining the distal esophagus—
Barrett’s esophagus.
• Adopt by Barrett himself—acquired, not
congenital disorder.
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.
TYPE
• Gastric fundic type resembling stomach
epithelium.
• Junctional epithelium resembling gastric cardia.
• Intestinal glandular epithelium characterized by
goblet cell.
• The intestinalized epithelium is most common and
importannt histologic type — predisposing patient
to the develop the adenocarcinoma of esophagus.
Pathogenesis
• Gastroesophageal reflux — leads to destruction of the
normal squamous lining of esophagus, and allow
subsequent cephalad migration of columnar gastric
lining to re-epithelized the injured area.
• Alkaline reflux — also involved, particularly in
developing complication.
• Chemotherapy — as cyclophosphamide, methotrexate,
5-FU.
• Congenital — fetal development the columnar
epithelium is replaced by squamous epithelium, island
of columnar epithelium persist, usually at proximal
esophagus, associated with GER.
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
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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.
Esophageal manometry and pH testing
• Diminished lower esophageal sphincter
pressure, poorer esophageal acid clearance
more frequent esophageal acid exposure,
time of distal esophageal pH less than 4 is
15-39%.
• Twice as high as patient with esophagitis
without Barrett’s esophagus, 10 fold higher
than normal.
Biomarkers
• Alteration in DNA content.
• p53 mutation.
• p27 inactived.
Complication.
Ulceration and stricture
• More in patient with Barrett’s esophagus（1015%） 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%.
Treatment
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.
Barrett’s ulcer
• Most heal with medical therapy — H2blocker, 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.