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Charlotte Patterson
The treatment and management of
Barrett’s Oesophagus
Barrett’s Oesophagus
 Affects the distal oesophagus
 Consequence of chronic pathological reflux of the gastric content
 Often asymptomatic, and found as a consequenece of
endoscopic investigation for other conditions.
Risk factor Literature
GORD (Eisen et al., 1997)
Obesity (El-Serag et al.,
2006)
Hiatial hernia (El-Serag et al.,
2006)
Absence of H. pylori
infection
(Goldblum et al.,
1998)
Pathophysiology
 Chronic exposure to gastric content leads to
intestinal metaplasia
 Cellular & DNA damage alters the differentiation
potential of proliferating epithelial cells.
 The metaplastic change is macroscopically visible
using an endoscope.
Squamous epithelium  Columnar epithelium
(distal oesophagus) (gastric cardia, fundus, upper intestine)
Pathophysiology cont.
Endoscopic changes in
BO
Histological changes in
BO
MOUTH
STOMACH
OESOPHAGUS
DUODENUM
SQUAMOUS EPITHELIUM
COLUMNAR EPITHELIUM
Pathophysiology cont.
 The intestinal metaplasia may be classified
histologically as:
 Non-dysplasic
 Low grade dysplasia (LGD)
 High grade dysplasia (HGD)
 In HGD, dysplastic cells are still confined by the
basement membrane. However, due to the large
numbers of dysplastic cells there is a high chance
of subsequent invasion of the submucosa, and
progression to adenocarcinoma.
Pathophysiology cont.
...So what?
 Individuals with this condition have a 30- to 50-
fold increased risk of developing oesophageal
cancer (adenocarcinoma). (O'Connor et al.,
1999).
 The 5 year survival rate with oesophageal cancer
is 9% (Kumar & Clark, 2008).
 ... This makes oesophageal cancer one of the
commonest causes of cancer related mortality.
Why diagnose Barrett’s?
 Part of the reason oesophageal cancer has such a high
mortality, is because 70% patients don’t present until the
disease is stage III or higher (TMN classification system)
 BO is one of the most important risk factors for
oesophageal cancer
 Therefore if BO is diagnosed and treated before it
becomes dysplastic, could the oesophageal carcinoma
associated mortality be reduced?
Staging of oesophageal cancer based on the TNM classification system
Stage of cancer Five year survival
I 80%
II 30%
III 18%
IV 4%
Treatment of Barrett’s?
 An American study in the 1990s by Cameron et
al. showed the prevalence of Barrett’s to be 0.5%
on autopsy.
 A more recent Sweedish study showed a
prevalence of 1.6% in a cohort of 3000.
 Prevalence of BO in patients with GORD is
significantly higher- 8-20% in Western countries.
 The risk of developing adenocarcinoma from BO
is relatively low, at 0.5% per patient year.
Treatment of Barrett’s cont.
 Treatment of everyone with the condition would
be unfeasible, and place too greater strain
financially on the NHS.
 Treatment is invasive, and isn’t preferable to
patients with asymptomatic Barrett’s.
Current management
 Non-dysplastic Barrett’s
 Endoscopic surveillance every 2-3 years
 Low-grade dysplasia
 Endoscopic surveillance every 2-3 years
 6-28% risk of developing HGD
 High-grade dysplasia
 Invasive surgical or endoscopic treatment
 2.2-11.8% risk of developing adenocarcinoma
 Adenocarcinoma
 Invasive surgical or endoscopic treatment
What is the treatment?
 SURGICAL
 Total oesophagectomy and lymphadenectomy
 20% post-operative mortality
 85% 5 year mortality
 £25,000- before any post-operative complications
 Therefore this treatment is far from ideal...
 Could it be more successful if the disease was treated when
less dysplastic?
o A very extreme treatment option for an asymptomatic
patient with LGD and only a 6-28% chance of
developing HGD.
o Financial burden on NHS would increase
What is the treatment cont.
 ENDOSCOPIC
 Ablation
 Destroy the affected tissue, allowing it to be replaced with
the normal squamous epithelium of the oesophagus.
 However, no sample of the tissue is obtained therefore
infiltration depth of the lesion may be underestimated, and
invasion of lymph nodes and blood vessels may not be
identified
 Therefore this shouldn’t be used as a stand-alone treatment
for HGD or adenocarcinoma.
 Resection
 Remove the mucosa and submucosa, leaving the
muscularis propria exposed.
 Confirm that the cancerous tissue has margins within the
resected lesion.
Endoscopic resection
 This technique has been used with high success rates
 Specialist centre in Wiesbaden, Germany involving 144
patients undergoing endoscopic resection for HGD showed
a 99% remission rate in patients, with a 98% 5 year
survival rate. (Pech et al. 2007).
 However, this wasn’t an RCT- these patients were selected
as they were considered ‘low-risk’ (ie. The cancer was
limited to the mucosal layer).
 Studies involving ‘higher-risk’ patients showed poorer
results.
 Reoccurrence is quite frequent, estimated at around 11%
(Peters et al, 2006). However, if patients attend follow-up
appointments, complications from this are minimised.
 Is this only treating ‘the tip of the iceberg’? Leaving behind
residual, potentially cancerous tissue? Could this
compromise the long-term prognosis, and chances of
actually ‘curing’ the cancer?
 No, if used successfully like in Wiesbaden Germany.
Endoscopy vs surgery?
 At present, most centres in the UK offer
oesophagectomy as first-line treatment for HGD and
adenocarcinoma.
 Endoscopic treatment is considered only if the patient
is considered un-fit for surgery, and as palliative
treatment.
 There has yet to be an RCT comparing the two.
 However, study using a decision analysis model
carried out based on data from non-RCTs showed:
 Endoscopic was more effective and less expensive than
surgical treatment.
 The cost of endoscopic resection was $17,000 and 4.88
Quality adjusted life years (QALY), compared with a cost of
$28,000 and 4.59 QALY for oesophagectomy.
(Pohl et al, 2009)
In conclusion...
 There are two main ways of treating high-grade
dysplasia.
 Oesophagectomy
 Endoscopic ablation or resection
 Oesophagectomy is the treatment of choice in the
UK, but it is expensive and has low success
rates.
 Endoscopic resection has been used successfully
in specialist centres, such as Wiesbaden,
Germany with excellent results.
 If this technique can be used successfully in other
countries, surely it is only a matter of time before
this technique is used with similar success rates
Thank you for listening!

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Barrett's Oesophagus - Treatment and Management

  • 1. Charlotte Patterson The treatment and management of Barrett’s Oesophagus
  • 2. Barrett’s Oesophagus  Affects the distal oesophagus  Consequence of chronic pathological reflux of the gastric content  Often asymptomatic, and found as a consequenece of endoscopic investigation for other conditions. Risk factor Literature GORD (Eisen et al., 1997) Obesity (El-Serag et al., 2006) Hiatial hernia (El-Serag et al., 2006) Absence of H. pylori infection (Goldblum et al., 1998)
  • 3. Pathophysiology  Chronic exposure to gastric content leads to intestinal metaplasia  Cellular & DNA damage alters the differentiation potential of proliferating epithelial cells.  The metaplastic change is macroscopically visible using an endoscope. Squamous epithelium  Columnar epithelium (distal oesophagus) (gastric cardia, fundus, upper intestine)
  • 4. Pathophysiology cont. Endoscopic changes in BO Histological changes in BO
  • 6. Pathophysiology cont.  The intestinal metaplasia may be classified histologically as:  Non-dysplasic  Low grade dysplasia (LGD)  High grade dysplasia (HGD)  In HGD, dysplastic cells are still confined by the basement membrane. However, due to the large numbers of dysplastic cells there is a high chance of subsequent invasion of the submucosa, and progression to adenocarcinoma.
  • 8. ...So what?  Individuals with this condition have a 30- to 50- fold increased risk of developing oesophageal cancer (adenocarcinoma). (O'Connor et al., 1999).  The 5 year survival rate with oesophageal cancer is 9% (Kumar & Clark, 2008).  ... This makes oesophageal cancer one of the commonest causes of cancer related mortality.
  • 9. Why diagnose Barrett’s?  Part of the reason oesophageal cancer has such a high mortality, is because 70% patients don’t present until the disease is stage III or higher (TMN classification system)  BO is one of the most important risk factors for oesophageal cancer  Therefore if BO is diagnosed and treated before it becomes dysplastic, could the oesophageal carcinoma associated mortality be reduced? Staging of oesophageal cancer based on the TNM classification system Stage of cancer Five year survival I 80% II 30% III 18% IV 4%
  • 10. Treatment of Barrett’s?  An American study in the 1990s by Cameron et al. showed the prevalence of Barrett’s to be 0.5% on autopsy.  A more recent Sweedish study showed a prevalence of 1.6% in a cohort of 3000.  Prevalence of BO in patients with GORD is significantly higher- 8-20% in Western countries.  The risk of developing adenocarcinoma from BO is relatively low, at 0.5% per patient year.
  • 11. Treatment of Barrett’s cont.  Treatment of everyone with the condition would be unfeasible, and place too greater strain financially on the NHS.  Treatment is invasive, and isn’t preferable to patients with asymptomatic Barrett’s.
  • 12. Current management  Non-dysplastic Barrett’s  Endoscopic surveillance every 2-3 years  Low-grade dysplasia  Endoscopic surveillance every 2-3 years  6-28% risk of developing HGD  High-grade dysplasia  Invasive surgical or endoscopic treatment  2.2-11.8% risk of developing adenocarcinoma  Adenocarcinoma  Invasive surgical or endoscopic treatment
  • 13. What is the treatment?  SURGICAL  Total oesophagectomy and lymphadenectomy  20% post-operative mortality  85% 5 year mortality  £25,000- before any post-operative complications  Therefore this treatment is far from ideal...  Could it be more successful if the disease was treated when less dysplastic? o A very extreme treatment option for an asymptomatic patient with LGD and only a 6-28% chance of developing HGD. o Financial burden on NHS would increase
  • 14. What is the treatment cont.  ENDOSCOPIC  Ablation  Destroy the affected tissue, allowing it to be replaced with the normal squamous epithelium of the oesophagus.  However, no sample of the tissue is obtained therefore infiltration depth of the lesion may be underestimated, and invasion of lymph nodes and blood vessels may not be identified  Therefore this shouldn’t be used as a stand-alone treatment for HGD or adenocarcinoma.  Resection  Remove the mucosa and submucosa, leaving the muscularis propria exposed.  Confirm that the cancerous tissue has margins within the resected lesion.
  • 15. Endoscopic resection  This technique has been used with high success rates  Specialist centre in Wiesbaden, Germany involving 144 patients undergoing endoscopic resection for HGD showed a 99% remission rate in patients, with a 98% 5 year survival rate. (Pech et al. 2007).  However, this wasn’t an RCT- these patients were selected as they were considered ‘low-risk’ (ie. The cancer was limited to the mucosal layer).  Studies involving ‘higher-risk’ patients showed poorer results.  Reoccurrence is quite frequent, estimated at around 11% (Peters et al, 2006). However, if patients attend follow-up appointments, complications from this are minimised.  Is this only treating ‘the tip of the iceberg’? Leaving behind residual, potentially cancerous tissue? Could this compromise the long-term prognosis, and chances of actually ‘curing’ the cancer?  No, if used successfully like in Wiesbaden Germany.
  • 16. Endoscopy vs surgery?  At present, most centres in the UK offer oesophagectomy as first-line treatment for HGD and adenocarcinoma.  Endoscopic treatment is considered only if the patient is considered un-fit for surgery, and as palliative treatment.  There has yet to be an RCT comparing the two.  However, study using a decision analysis model carried out based on data from non-RCTs showed:  Endoscopic was more effective and less expensive than surgical treatment.  The cost of endoscopic resection was $17,000 and 4.88 Quality adjusted life years (QALY), compared with a cost of $28,000 and 4.59 QALY for oesophagectomy. (Pohl et al, 2009)
  • 17. In conclusion...  There are two main ways of treating high-grade dysplasia.  Oesophagectomy  Endoscopic ablation or resection  Oesophagectomy is the treatment of choice in the UK, but it is expensive and has low success rates.  Endoscopic resection has been used successfully in specialist centres, such as Wiesbaden, Germany with excellent results.  If this technique can be used successfully in other countries, surely it is only a matter of time before this technique is used with similar success rates
  • 18. Thank you for listening!

Editor's Notes

  1. The darker discolouration shows