2. Definition
A change in the normal squamous epithelium
of the oesophagus to specialized intestinal
metaplasia
Playford RJ. New British Society of Gastroenterology guidelines for the
diagnosis and management of Barrett’s esophagus
Gut 2006;55:442-3
4. Etiology
Combined acid and bile reflux
> 50% of patients with GERD had abnormal
levels of acid and bile in the oesophagus
Barrett’s esophagus patients have the highest
level
Fein M. BrJ Surg 2006; 93: 1475-82
6. Risk of Adenocarcinoma
0.25 to 0.4% per year
Nondysplasic : 3.86/1000 person years
Low-grade dysplaia: 7.66/1000 person years
High-grade dysplasia
Occult carcinoma: 30%-40% of patients
14.1/100 person years
Sharma P. Clin Gastroenterol Hepatol 2006; 4: 566-72
Buttar NS. Gastroenterology 2001; 120: 1630-9
7. Endoscopic Evaluation
Prague classification
the maximal length (M)
(including tongues) of
Barrett esophagus
length of the
circumferential Barrett
segment (C)
For future endoscopic
comparison
Sharma P. Gastroenterology 2006; 131: 1392-9
8. Biopsies
Seattle protocol
4 quadrant jumbo bx at 1cm intervals throughout
whole length of Barrett’s
Separate target bx of any irregularities
(nodules/erythema/ erosions)
Reid BJ. AmJ Gastroenterol 2000; 95: 3089-95.
11. Acid Suppression with
Surveillance
Acid suppression will not eliminate risk of
adenocarcinoma/ consistent regression of
Barrett’s
Degree of dysplasia Surveillance OGD interval
Non-dysplastic 3-5 year
Low grade dysplasia 6-12 months
High grad dysplasia Interval 3 months (if patient not
receive invasive therapy)
? Duration and dosage
of PPI (indefinite)
?optimal frequency of
surveillance
12. Anti-reflux Surgery
Fundoplication eliminates acid and bile reflux
in > 90% of patients with Barrett’s
oesophagus
Meta-analysis: 15.4% of patients undergone
surgery will have regression of Barrett’s vs.
1.9% medically managed patients
Swedish Cohort study showed that RR of
adenocarcinoma in patients undergone
surgery was 14.1 vs. 6.3 for medical treatment
Oelschlager BK. Ann Surg 2003; 238: 458-64.
Chang EY. Ann Surg 2007; 246: 11-21.
Lagergren J. Gastroenterology 2010; 138: 1297-301
Reduce risk of adenoCA ?
Mixed evidences so far
13. PPI vs fundoplication
Surgery can definitely treat reflux-related
symptoms, but its role in protection against
adenocarcinoma should be cautious
Effectiveness in eliminating reflux symptoms
Co- morbidities
Patient’s choice/ compliance
Medications S/E
14. Photodynamic Therapy
Injecting a light-sensitizing drug into patient,
then expose the portion of oesophagus to a
specific wavelength
Found NOT effective in eliminating Barrett’s
‘Buried glands’: a layer of normal-appearing
squamous epithelium is present but under
this layer, Barret’s metaplasia still present
Stricture
Phototoxicity
Menon D. BMC Gastroenterol 2010; 10: 111.
15. Argon Plasma Coagulation
Systemic review: more effective than PDT, 3-
month complete eradication 80%
Less complications like stricture or bleeding
Odynophagia 10%
LiYM. Dig Dis Sci 2008; 53: 2837-46.
16. Radiofrequency Ablation
One of the best studied method
Applies bipolar electrical energy to mucosal
surfaces, 10J for 1 second mucosa is ablated
to submucosal level
17. Radiofrequency ablation
Need standardized FU as complete ablation
with single treatment in only 70% of patients
FU OGD 3 months and 1 year, if not complete
ablated repeat RFA
18. Radiofrequency ablation
Shaheen NJ (2009): Multicentre RCT
Can eliminate Barrett’s oesophagus with high grade
dysplasia and reduce risk of oesophageal carcinoma
Wani S (2009): Meta-analysis
Reduction in carcinoma progression in high-grade
dysplasia
Shaheen NJ (2011): Long term results
3 years follow-up: complete eradication persist in
96% patients with high-grade dysplaia
Adenocarcinoma occurred in one per 181 patient-
years of follow-up
19. Radiofrequency ablation
Promising results
S/E : esophageal stricture,GIB, chest pain
Sustaintially lower than those in
photodynamic therapy
Long term data needed
20. Cryoablation
Endoscopically directed spray of liquid nitrogen
at -196oC
Complete eradication of high grade dysplasia
occurs in 68-97% of patients
Not well studied as RFA
?Treat patient refractory to RFA
DumotJA.Gastrointest Endosc 2009; 70: 635-44.
Shaheen NJ.Gastrointest Endosc 2010; 71: 680-5.
21. Endoscopic Mucosal Resection
when a visible nodule is present
or only a short segment of Barrett’s
is seen
substantial tissue for pathologist
treatTis orT1a adenocarcinoma
Can combined with RFA
With submucosal invasion,
20% risk of LN met
If confined to mucosa ,<1% LN
met
22. Endoscopic therapy
No single endotherapy achieve complete
eradication without complications
Recurrence
For mucosal lesion
Buried metaplasia
23. Esophagectomy
‘gold standard’ for high grade dysplasia and
early adenocarinoma
20-40% of patients harbour early
adenocarcinoma in HGD (old data)
Mortality can be as low as 1% in high vol
centre
Significant morbidity
For multifocal , too extensive HGD /
intractable HGD /suspicious of carcinoma
25. Take Home Messages
Barrett’s esophagus is a pre-malignant
condition
Diagnosis relies on both endoscopic and
histological findings
Management should be based on risks
stratification
Emerging evidence on the use of endoscopic
therapy
Treatment should be individualized
Editor's Notes
Normal eso squamous mucosa
Intestinal metaplasia (goblet cells)
Difficult to truly know prevalence as many barretts individual are asymptomatic and never be evaluated
Mucosal injury most common in mixed acid and bile exposure. Followed by acid alone and uncommon for bile alone (P<0.001)
Salmon color epithelium projected into tubular esophagus (projection can be tongues of tissue/ circumferential involvement of mucosa)
-4 quadrant jumbo biopsies at 1 cm intervals throughout length of Barrett's esophagus (and inclusive of any neosquamous re-eepithelialized tissue growth and cardia)
irregularities (tiny nodules, patches of friability/erythema, erosions, ulcers, strictures, or regions appears fixed and or poorly distensible)
Currently, white light high definition endoscopy and chromoendoscopy help in localizing lesions
Tx rationale barrett mucosal disease before it progress to CA / crossing submucosa–removal of disease mucosa suffix
Role of endoscopic ablation in non-dysplastic/ low grade dysplasia is less clear
No reliable data on tx length
-some keep patients on PPI indefinitely. Supra-therapeutic dose (for control of GERD) solely for chemoprevention is not warranted
Optimal frequency of surveillance has not yet been determined, most recommend as above chart
adenoCA discovered while screening for Barretts are early stage lesions and have a gd prognosis (5 year suvival >85%)
Meta-analysis found no difference between fundoplication and medical treatment in prevention of adenocarcinoma
Stricture esp in long segment
Balloon based radiofrequency device for circumferential ablation
RFA advantage : treat larger surface area than other thermal techniques, also true for focal disease
(contact technique but not point technique)
Usually visible nodule has higher chance of ca
Endoscopic resection followed by thermal ablation should be treatment of choice
EUS to determine pass thro submucosa
Thro submucosa,risk of LN met >20%
EMR ~2 cm size specimen in each attempt while ESD can remove specimen en bloc regardless of size
Traditionally esophagect gold standard for early ca and HGD
Old data show 20-40% occult CA in HGD. Only 12 % in Jennifer Chennat at el 20101(gastrointest enodoscopy clin N AM 21 (2011)119-133
Vagal sparing esophagectomy , laparoscopically
Ablation or resection not suitable for multifocal/ too extensive disease
After esophagect, life long reflux/ regurg/ aspiration
With potential early and long term cx and magnitude of procedure, usu discourage patient from doing esophagect
Esophagect is a 1 shot procedure
Surgery vs ablation for high grade/ early CA
No RCT yet . All non randomized trails - all no significant difference in survival
HGD –procedure shift from esophagectomy to endoscopic ablative /resection
Flat HGD – ablation + PPI
Nodular HGD EMR/ ESD +PPI
Ablative therapy for metaplasia w/o dysplasia ? (non dysplastic barretts develop CA at only 0.5% per year, no study established that endoscopic ablation decreases risk)
Also need surveillance OGD afterwards as we dunnno the chance of buried metaplasia and regrowth of barretts (review stuart et al surg oncol clin N AM 18 2009 509-521) similar for LGD- not much evidence on tx by ablative therapy, more outcome needed to support recommendation. Some have Spontaneous regression
Intractable HGD/ suspicious of carcinoma – esophagectomy
Some study on cost perspective- HGD most cost effective tx by RFA, EMR cost preferred than esophagectomy for early BE
Risk stratification (no dysplasia/ LGD/ HGD)
When to treat : currently no evidence for ablation in non dysplastic/ LGD - surveillance +PPI
Surgery vs ablation equally effective – the best mx depends on patient characteristics , preference, local expertise. Multiple comorbities- endoscopic tx