Editing Barrett's oesophagus


"Endoscopically-visible segment of metaplastic columnar mucosa in the oesophagus, with intestinal metaplasia proven histologically."

* Note differing definitions     between UK and USA - requirement of intestinal metaplasia (as indicated by     goblet cells) is uncertain. USA says goblet cells required, UK says not     required.

== '''Risk factors''' ==

* Complication of GORD - GORD     is the ONLY cause of BO

== '''Screening''' ==

* Not currently recommended in     Australia, but can be done overseas as per below
* Indications for screening to     look for Barrett's: (if multiple risk factors and have had GORD for >5     years)
** Age >50
** Male
** White
** Hiatal hernia
** Obesity
** Nocturnal reflux
** Smoker
** First-degree relative with      Barrett's and/or adenocarcinoma
* Only need to screen each     patient once.
* If they have oesophagitis,     give PPI for 3/12 and screen again


== '''Pathophysiology''' ==

* Dysplasia in Barrett's is     characterised by cytologic malignant changes including atypical nuclei,     increased mitoses, and lack of surface maturation
* Dysplasia is most common     closer to GOJ in a long segment of Barrett's
* HGD is distinguished from LGD     by more prominent cytologic or architectural derangements
* Remains dysplasia as long as     it is confined to the epithelium without invasion of the basement     membrane, regardless of the degree of abnormality
* Histological grading is based     on the Vienna classification system - non-dysplastic, indeterminate, LGD,     HGD, intra-mucosal carcinoma
** Lots of intra-observer      variation. In particular, LGD from general pathologists is downgraded to      non-dysplastic by specialist pathologists in 73% of cases
** Indefinite for dysplasia      means equivocal for inflammation or dysplasia - 11.4% pooled annual risk      for progressing to LGD and 0.6% for progression to carcinoma
* Precursor for oesophageal     adenocarcinoma
** Non-dysplastic - 0.3 per 100      person-years
** LGD - 0.5
** HGD - 6.6
** Overall incidence of      oesophageal adenocarcinoma in BE patients is about 40x the general      population
* Long segment is >=3cm -     significantly higher risk of progression to carcinoma
* Short tongues     <1cm/'variable Z-line' were previously called ultra-short segment     Barrett's, but do not constitute increased malignancy risk and no need to     biopsy if no concerns for dysplasia

== '''Evaluation:''' ==

* Careful endoscopy - white     light and NBI are both useful
** Suspect when GOJ (proximal      extent of rugae) is >=1cm distal to the z-line
** Barrett's has a      characteristic salmon pink colour and velvety texture
** Firstly identify the segment      of columnar epithelium, and also look for areas of irregularity within it
** Use Prague classification      system (see 'endoscopy' topic)
** Note hiatal hernias
** Seattle protocol for      biopsies
* Oesophagitis + Barrett's
** If LA C or D oesophagitis is      found, the pathologist will have trouble identifying dysplasia and a      diagnosis of 'indeterminate' is likely
** If no concerns for cancer,      put them on high-dose PPI and re-scope in 6-8 weeks
* Irregular z-line:
** Found in 10-15% of patients
** When the SCJ lies above the      GOJ, but without any confluence, forming tongues shorter than 1cm, and      thus does not fulfil criteria for BO
** It can harbour histological      intestinal metaplasia, but the progression rate to BO is low, let alone      to malignancy, so no further evaluation or screening is recommended

== '''Principles of management:''' ==

# '''Therapy for GORD'''
# '''Prevention of progression/treatment of BE'''

== Management and surveillance: ==

=== Flat or nodular lesion     present within Barrett's: ===

** Refer to centre with EMR/ESD      for resection

=== '''Barrett's     <1cm''' ===

** No increased risk of      malignancy
** No clear guidelines, but      probably don't need to do another scope

=== '''Non-dysplastic     BE''': manage as     for GORD ===

** Symptom relief
** Continue PPI indefinitely
** Don't recommend anti-reflux      surgery just because of theoretical risk of progression - incidence of      cancer appears to be low
** If can't control symptoms      with lifestyle and medication, then they need anti-reflux surgery      (exactly same as uncomplicated GORD)
** Radiofrequency ablation is      unproven in this population
** '''Surveillance:'''
*** Non-dysplastic BE - 3-5       yearly - but could do much more frequently to limit progression to that       which can be treated endoscopically - some UGI surgeons do yearly scopes
**** If short segment        (<3cm), thoroughly biopsied, and no dysplasia, surveillance every        five years (10% risk of dysplasia)
**** Long segment every three        years (31% risk of dysplasia)
*** Consider stopping       surveillance in elderly or unfit patients, similar to NBCSP

=== '''Indefinite     for dysplasia''' ===

** BD PPI
** Re-scope Seattle protocol      3-6/12
** If still indefinite, review      with experienced pathologist and either surveillance every 12 months or      referral to Barrett's centre
** Most will regress to      non-dysplastic

=== '''Low-grade     dysplasia''' ===

** Repeat endoscopy ASAP with      Seattle protocol if you didn't do it initially - need to exclude more      advanced disease
** Need to review slides with      experienced pathologist
** Either start on PPI or      increase existing dose
** American College of      Gastroenterology suggests either endoscopic eradication (then follow-up      endoscopy in 6 months) or surveillance every six months for one year and      then annually until reversion
*** Most sensible way is       probably to check persistence, and refer for ablation if persistent
** Can be offered anti-reflux      surgery - given that most patients with LGD regress after surgery
** If persistent, may need      mucosal ablation

=== '''High-grade     dysplasia''' ===

** Review slides with      experienced pathologist
** '''Indication      for intervention'''      - ideally RFA
** Most get endoscopic therapy,      followed by surveillance gastroscopy three months later
** Careful repeat biopsy - look      out for focus of invasive carcinoma - use every imaging modality      available - white light, NBI, acetic acid
** Small lesions - endoscopic      resection - ideally take full thickness of mucosa and submucosa
** Can evaluate lesions larger      than 1-2cm for invasion using EUS - key point would be whether it is T1a      or T1b
** '''If HGD or      T1a (without LVI), options are oesophageal preservation therapy vs      oesophagectomy'''
*** Oncologically equivalent,       but long-term surveillance and multiple initial scopes required, and       recurrence is a risk
*** Oesophagectomy historically       gets good results in this group, with mortality under 1%
*** However, endoscopic       treatment and surveillance is much better now

== '''Endoscopic therapy''' ==

* Goals are removal of BE     epithelium, while preserving overall integrity of the oesophagus and     accurately staging dysplasia or invasive disease
* Should have close     surveillance and PPI afterwards
* Beware the risk of 'buried     glands' - areas of Barrett's epithelium hidden beneath areas of new     squamous epithelium, even if the risk of malignancy in those glands     appears to be low
* '''Radiofrequency     ablation'''
** Most commonly used      endoscopic therapy
** This is the HALO device,      although I think it has been renamed now to 'Barrx'
** Much more effective than      photodynamic therapy with a lower stricture and overall complication rate
** Delivered with either a      circumferential balloon or an electrical plate. The treated mucosa is      replaced by neosquamous mucosa. The standard ablation program uses two      double pulses of 12 J/sq cm.
** AIM-II trial - 81% of      patients with HGD and 90% of patients with LGD had eradication of      dysplasia. 4% had their dysplasia progress to a higher grade.
* '''Argon plasma     coagulation'''
* '''Cryotherapy'''
** Generally well tolerated      with little pain and low stricture rates
** Does not require the probe      to be in contact with tissue
** Use either a balloon or      endoscopic spray catheter to deliver liquid nitrogen
** Eradicated LGD and HGD at      91% and 81% respectively in one study
** Can be used as salvage      therapy after failed RFA
* '''Photodynamic     therapy'''
* '''Endoscopic     mucosal resection'''
** Best for visible segments
** Commonly use 'Duette' system      (Cook)
* '''Endoscopic     submucosal dissection'''
** Better with >2cm
** Best option for cancer
* '''Surveillance     after eradication'''
** Previous HGD: 1, 2, 3, 4, 5,      7, 10 years after treatment
** Previous LGD: 1, 3, and 5      years after treatment

[[Category:UGIS]]