1. GENERAL THORACIC SURGERY CHAPTER 141
BARRETT’S ESOPHAGUS
GENERAL THORACIC SURGERY
CHAPTER 141

2. 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.

3. 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.

4. 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.

5. 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.

6. Prevalence 2% of patient undergoing panendoscopy.
44 % patient of peptic stricture with Barrett’s esophagus.
27/
Autopsy 376/
Most barrett’s esophagus are asymptomatic.

7. Clinical feature Asymptomatic. GER and complication.
Heartburn, regurgitation.
Dysphagia from stricture or carcinoma.
Tobacco and alcohol use.

8. Radiology Difficult to diagnose by radiography.
Sliding hiatal hernia with esophagitis.

10. 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.

11. 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.

12. Biomarkers
Alteration in DNA content.
p53 mutation.
p27 inactived.

13. Complication.

14. 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.

16. Dysplasia Low and high grade.
Loss pf nuclear polarity, hyperchromatism, nuclear enlargement, stratification, pleomorphism, abnormal mitoses.
Distinguish high and low grade is difficult.

17. Adenocarcinoma
Distinguish adenocarcinomna in Barrett’s esophagus from carcinoma of cardia is difficult.
times the risk of normal population.
1 case per 100 patient-year, annual risk 1%.

19. Treatment

20. 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.

21. 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.

22. 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.

23. 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.

25. 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.

26. Adenocarcinoma Esophagogastrectomy. Higher respectability — 94-100%.
Long term survival similar — 20% in 5-year.