BARRETT

1
BARRETTS 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 esophagusBarretts esophagus.
• Adopt by Barrett himselfacquired, 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 Barretts
  esophagus.
• 27/100000.
• Autopsy 376/100000.
• Most barretts 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.

9
(No Transcript)
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
  Barretts 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 Barretts 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.

15
(No Transcript)
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 Barretts
  esophagus from carcinoma of cardia is difficult.
• 30-125 times the risk of normal population.
• 1 case per 100 patient-year, annual risk 1.

18
(No Transcript)
19
Treatment
20
Benign Barretts esophagus

• Asymptomatic and uncomplication not require
  treatment.
• Medical treatment of GER infrequently regression
  the Barretts 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 Barretts 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
Barretts 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.

24
(No Transcript)
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.