Honorary Senior Clinical Lecturer, University of Sheffield

Consultant Gastroenterologist

Barnsley Hospital NHS Foundation Trust, UK

elmuhtady.said@nhs.net©4th SSG conference, Jan 2014

©4th SSG conference, Jan 2014, SAID EM

Definition

Surveillance

Non-dysplastic BO

Dysplastic BO

Early oesophageal cancer

Summary

©4th SSG conference, Jan 2014, SAID EM

Br J Surg. 1950-1951;38:175-182.

Norman R. Barrett 1903-1979

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“I submit that most of these cases are in truth examples of : congenital short oesophagus in which a part of the stomach extends upwards into the mediastinum.”

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• Change in the type of cells within the epithelial layer of the lower oesophagus.

• The leading theory is response to chronic GORD [positive adaptation] as columnar epithelium is better able to withstand acidity.

• Oesophageal intestinal metaplasia or columnar lined oesophagus without metaplasia.

What is Barrett’s oesophagus?

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• "an endoscopically apparent area above the esophago-gastric junction that is suggestive of Barrett’s esophagus (salmon-colored mucosa) which is supported by the finding of columnar lined esophagus on histology”

• “displacement of the squamo-columnar junction proximal to the gastro-esophageal junction with histological evidence of specialized intestinal metaplasia on biopsy specimens.”

Definition

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Wang, K. K. & Sampliner, R. E. Updated guidelines 2008 for the diagnosis, surveillance and therapy of Barrett's esophagus. Am. J. Gastroenterol. 103, 788-797 (2008).

Playford, R. J. New British Society of Gastroenterology (BSG) guidelines for the diagnosis and management of Barrett's oesophagus. Gut 55, 442 (2006).

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“Barrett’s oesophagus is defined as an oesophagus in which any portion of the normal distal squamous epithelial lining has been replaced by metaplastic columnar epithelium, which is clearly visible endoscopically (≥1 cm) above the GOJ and confirmed histopathologically from oesophageal biopsies”

BSG guidelines 2013(Recommendation grade C)

Definition

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©4th SSG conference, Jan 2014, SAID EM

• To detect patients at greater risk of progressing to OAC at early & curative stage.

Aim of Barrett’s Surveillance

©4th SSG conference, Jan 2014, SAID EM 1-Van der Veen AH et al, GUT, 1989

• Although the risk of developing OC increased at least 30-fold above the general population, the absolute risk of developing cancer is low1

.

• Surveillance is based upon the assumptions that BO adversely influences survival & that surveillance can reduce mortality.

• Survival benefit in patients undergoing surveillance has not been demonstrated in randomized prospective trials.

• Current evidences base are from comparative studies and epidemiological retrospective cohort studies, grade III.

Controversies of Surveillance

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• AspECT trial Aspirin and esomeprazole chemoprevention in Barrett's metaplasia.

• BEST trial Barretts Oesophagus Screening Trial

• BOSS trial Barrett’s Oesophagus Surveillance Study.

• SURF Trial Surveillance with Radio-Frequency Ablation of Barrett’s

osophagus with Low-Grade Dysplasia

Controversies of Surveillance

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• Provide up to date practical and evidence base recourses for management of Barrett’s oesophagus and related early neoplasia, based on systemic review of literature up until Dec 2012.

BSG guidelines 2013

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Barrett’s oesophagus in Sudan

• Data suggest that BO is rare in all regions of sub-Saharan Africa

• A study from Egypt examining 1000 patients with chronic GORD symptoms found the presence of BO in 7.3%.

• heartburn

105

• Reflux oesophagitis

47• Barrett’

oesophagus

5

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Non-dysplastic Barrett’s

Oesophagus

Low grade dysplasia

LGD

High grade dysplasia

HGD

T1M oesophageal

adeno-carcinoma

0.5%

10%40%

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Non-dysplastic Barrett’s

oesophagus

Non-dysplastic BO

©4th SSG conference, Jan 2014, SAID EM 1-Bhat S et al, J Natl Cancer Inst, 2011

Frequency of surveillance:BO without IM <3 cm: DischargeBO with IM <3 cm: 3-5 yrsBO of 3 or more cm: 2-3 yrs

Short segment of columnar epithelium with no IM have an extremely low risk of malignancy

(~0.05% per annum)1.

Non-dysplastic Barrett’s

oesophagus

Non-dysplastic BO

Seattle Protocol Multiple samples, High cost

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Biopsy protocol:Quadrantic 2cm Biopsy protocol Sampling of any visible lesion.

Non-dysplastic BO surveillance flow chart BSG guideline 2013©4th SSG conference, Jan 2014, SAID EM

Low Grade

Dysplasia LGD

Low grade dysplasia LGD

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The diagnosis should be confirmed by two pathologists

Category 1 Negative for neoplasia/ dysplasia

Category 2 Indefinite for dysplasia

Category 3 Low grade dysplasia

Category 4 High grade dysplasia/ Carcinoma in situ

Category 5 Invasive neoplasia

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Revised Vienna classification1

1-Schlemper RJ et al, Gut 2000

Low Grade

Dysplasia LGD

Low grade dysplasia LGD

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The diagnosis should be confirmed by two pathologists

Frequency of surveillance: every 6 months

Endoscopic therapy?

• LGD correlate with higher risk of progression to cancer.

• Unclear whether this warrant endoscopic intervention.

• Clinicians may choose to treat some patients with ablationwhen dysplasia is persistent or multifocal on individual basis.

Low Grade

Dysplasia LGD

Low grade dysplasia LGD

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RFA

• Overall outcome: a lower risk of disease progression in all patients treated with RFA, but subgroup analysis in LGD patients failed to show a significant advantage from treatment.

• SURF Trial: RFA compared with endoscopic surveillance is awaited.

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Radio Frequency Ablation RFA

Shaheen NJ, N Eng J Med, 2009

Low Grade

Dysplasia LGD

Low grade dysplasia LGD

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The diagnosis should be confirmed by two pathologists

Frequency of surveillance: every 6 months

Based on current evidence, ablation therapy cannot be

recommended routinely until data from RCT are available.

Indefinite for

dysplasia

Indefinite for dysplasia

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Pathologists unable to make definite diagnosis of dysplasia

? inflammation

Frequency of surveillance: every 6 months

Treat with high dose PPI

v

High Grade

Dysplasia HGD

High grade dysplasia HGD

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Confirm diagnosis:Expert HRE to detect visible lesion

Second pathologists

• Chromoendoscopy

• Autoflorescence

• Narrow band imaging

• Acetic acid

High Resolution Endoscopy

HRE should be used to maximize dysplasia detection. grade C

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aceticالخل acid chromoendoscopy

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Acetic Acid Spray Is an Effective Tool for the Endoscopic Detection of Neoplasia in Patients With Barrett's Esophagus

v

High Grade

Dysplasia HGD

High grade dysplasia HGD

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Confirm diagnosis:Expert HRE to detect visible lesion

Second pathologists

MDT discussion

Therapeutic intervention?

HGD and early cancer T1a/T1b

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HGD and

early cancer

Imaging for HGD & T1 cancer

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In selected cases, EUS +/- FNA if :1. Endoscopist cannot exclude

advanced stage of nodular lesion.2. Visible lymph nodes in selected

cases of T1b. (Grade C)

Before ER,CT/PET-CT no role in stagingEUS can overstage/ understage. (Grade B), Not recommended

v

HGD and

early cancer

Ablation Therapy

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Flat HGD/intermucosal cancer without visible lesion should be managed with ablation therapy.

1-BSG guideline 2013

RFA has better safety, side effect profile and comparable efficacy1.

All ablation modalities improve eradication compared with surveillance for HGD (grade Ib)

Radio Frequency Ablation RFA

v

HGD and

early cancer

Endoscopic Resection

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Cap & snare with submucosal injBand ligation without submuc inj

Equally effective.2

Patient at high surgical risk, ER can be offered as an alternative.

Therapy of choice for dysplasia + visible lesion and T1a OAC.1

1-Canio M,World J Gastroentrol, 20052-Pouw RE,Gastrointest Endosc,2011

vEndoscopic Resection

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v

High Grade

Dysplasia HGD

Surgery

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Treatment of choice for T1b due to significant risk of LN metastasis.

Oesophagectomy should be performed in high volume specialized centers to reduce mortality.

No sufficient data to recommend surveillance following oesophagectomy.

v

High Grade

Dysplasia HGD

HGD and early cancer T1a/T1b

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Confirm diagnosis:Expert HRE to detect visible lesion

Second pathologists

MDT discussion

Flat lesion-RFAVisible lesion-ER

HGD/T1a cancer:RFA after resectionT1b cancer: surgery

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MDT discussion

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Flow chart for the management of Barrett’s oesophagus.

BSG guideline 2013

HGD

v

• IM is not required for the diagnosis of BO, but impact on surveillance.

• Standard dataset in endoscopic and histopthologicalreporting.

• Consensus diagnosis of dysplasia.

• Surveillance for non-dysplastic Barrett’s hinges on IM and length.

• Routine CT & EUS not required in staging of early Barrett’s neoplasia.

• Communication through MDT& with patient essential

Summary of the main changes

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v

• Controversial due to lack of RCT.

• Current retrospective studies indicates survival advantage.

• On going trials.

• BSG guidelines provides up to date practical and evidence base recourses for management of BO and early oesophageal cancer and should be the gold standard.

Conclusion

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©4th SSG conference, Jan 2014, SAID EM

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