BARRETT’S ESOPHAGUS GENERAL THORACIC SURGERY CHAPTER 141

BARRETT’S ESOPHAGUS

GENERAL THORACIC SURGERY

CHAPTER 141

HISTORY

• Norman Barrett(1950) — congenitally short esophagus with an intrathoracic stomach.

• Allison and Johnstone (1953) and Lortat-Jacob (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

• 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 （ 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%.

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 — H2-blocker, 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.