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Dysplasia and cancer classifications: “Negative for dysplasia”. ”Indefinite for dysplasia”. “High grade dysplasia”. ”Intermucosal adenocarcinoma”. “Invasive adenocarcinoma”.
Barrett’s Oesophagus
1. Path reporting types Grades 0-No CLO/IM 1-CLO/no IM 2-CLO plus IM BO develops in <1 year with no progression
Barrett’s Oesophagitis
Intestinal Metaplasia
Low Grade Dysplasia
High Grade Dysplasia
Adenocarcinoma
10%
5%
15% over 2 yrs 50%
Risk of adenocarcinoma 0.6 %/yr if experts disagree or 50% if 3 experts agree Rate of cancer is 5%/yr Management of Barrett’s
Patients need PPI .
Surveillance endoscopy:
-If gastric metaplasia and <3cm rpt OGD then?d/c
-If IM and <3cm then rpt OGD 3-5 yrs
-If >3cm rpt OGD 2-3 yrs regardless of IM
-PPI’s cause partial BO regression with squamous islands.
Management of High Grade Dysplasia Options: Oesophagectomy. Endoscopic ablative therapies — Patients are then maintained on PPI. Radiofrequency ablation —using balloon causing circumferential or focussed Barrett’s eradication. Photodynamic therapy which is better than omeprazole alone for eradicating dysplasia and preventing cancer. Endoscopic mucosal resection. 2. Classified by
Length
a Long segment >3cm
b Short segment < 3cm (more common often asympto
-
matic
c Intestinal metaplasia at the cardia
2. Classified by histology
-Junctional type epithelium
, Pitted surface and mucus-
secreting cells (looks like gastric cardia)
-Gastric fundic-type epithelium
Pitted surface and mucus-
secreting cells and a deeper glandular layer containing chief
and parietal cells (looks like gastric fundus)
-Specialized intestinal metaplasia
(= specialized columnar
epithelium), which has intestinal-type crypts lined by
mucus-secreting columnar cells and goblet cells (best way to
distinguish from other types) and villi.
Can also have gastric-type cells, small intestinal-like cells, and
colonic-like columnar cells, endocrine and Paneth cells.
Indistinguishable histologically from IM type II or III of the
stomach.
The goblet cells of specialized intestinal metaplasia contain
acidic mucins (sialomucins and sulfomucins) stain with Alcian
blue +/- colonic-like mucins -stain with high-iron diamine.
IM more important than gastric metaplasia for cancer risk and
likely to be present in long segment BO.
Management of Low
Grade Dysplasia
If LGD then 6 monthly biopsies are
needed.
If LGD is not found on repeat
biopsies, then yearly endoscopy is
warranted until no dysplasia is
present on 2 consecutive annual
endoscopies.
Radiofrequency ablation can be
considered in selected cases
3-CLO + no IM-circumferential 4-CLO + IM-circumferential B Combination with endoscopic diagnosis for CLO C In keeping but not specific for CLO D No evident CLO Barrett’s subtypes:
Methods of assessing dysplasia in Barrett’s Autofluorescence endoscopy for Barrett's oesophagus are of two types-Light-induced fluorescence spectroscopy (LIFS) and Autofluorescence endoscopy (AFE). The role of autofluorescence is unclear. Narrow band imaging may be useful in Barrett's oesophagus to identify irregular mucosal pattern and abnormal vasculature. Zoom endoscopy provides higher definition. Spectroscopy (which is OCT based) is in development. RGB filter Seperates white light into primaries CCD Device CCD device detects reflected light Blue light reflects superficial mucosa and vessels (Hb absorbs blue light) Oesophageal adenocarcinoma risk 0.5%/year
Risk factors for conversion from reflux to Barrett's: Hiatus Hernia. LOS failure (90%). Peristaltic failure (70%). High acid exposure. Impaired mucosal sensitivity. Risk factors for conversion of Barrett's to IM: Being > than 45 years old. Having > 8cm length of Barrett's. Early onset GORD. Long duration of reflux. Having duodeno-oesophageal reflux. Study 1 : HGIN exhibited at least irregular mucosal patterns, irregular vascular patterns, or abnormal blood vessels. Barrett's definition and epidemiology
Barrett’s is defined as any part of the normal squamous lined oesoph
-
gus is replaced with metaplastic columnar epithelium above the GOJ
(3cm).
The average age at diagnosis is55.
Barrett’s is rare in blacks and asians.
The M:F prevalence is 2:1.
The prevalence is 2% but10% if the patient has heartburn.
The endoscopic sensitivity is > 80 %..
Diagnostic Criteria include
columnar epithelium in the distal oesophagus
(accuracy 80%).
Intestinal metaplasia is necessary for the diagnosis in the US only.
The endoscopic measurement is given by Prague staging consisting of C
(distance to circumferential Barrett’s from GOJ) and M (distance of Barrett’s
tongues from GOJ) distances.
May not eradicate all dysplasia, and may hide metaplasia under healed squamous tissue 15 % of PDT patients still develop esophageal cancer. PDT can cause strictures Written by Dr Sebastian Zeki
Reflux oesophagitis Methods of describing Barrett’s endoscopically 1. Prague criteria (C=circumferential proximal margin M = proximal limit of tongues. Both measured above the hiatus hernia (measured as the distance from the top of the gastric folds to the Z-line). 2. Paris criteria - to describe lesions- see early gastric cancer. Should all be assessed with HD scope and mucolytics. Spend 1min/cm Dont over-insufflate Most lesions between 12 and o’clock CLO tongue should be at least 1cm to be called Barrett’s. Management of Indefinite for dysplasia Rebiopsy at 6 months.
All these patients need high res endoscopy
Atypia with ulcer or inflammation OR if surface not visible OR not mature (last one= Basal crypt dysplasia- managed as per LGD Screening Barrett’s
Consider in high risk groups (symptomatic white, obese males or those with FDR with oesophageal ca or Barrett’s. Methods include endoscopic or cytosponge/ biomarkers in development Ideal lesions: HGD/IMC <3cm in size Good tumour differentiation No lymphatic/ vascular invasion
Can be done with a) lift+cut b) Band ligator c)En bloc resection. ER+ RFA (seperate sessions) better than ER alone.
