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BY-Aman Kailash Setiya
What is Barrett’s Esophagus?
 The esophagus gets a tissue
lining similar to that of the
intestines
 The muscle becomes rougher
 The cells that are normally
found in the intestine replace
the normal esophagus cells
Estimated prevalence of Barrett’s esophagus
 6-12% of patients who undergo EGD for GERD.
Short-segment BE: 6-12%
Long-segment BE: 1-5%
 1-2% of unselected patients who undergo EGD
 Most cases go undetected in the general
population [Autopsy data]. Perhaps 5% of patients
with Barret esophagus are currently being
diagnosed.
Symptoms of Barretts esophagus
 There are no specific
symptoms, they vary per
person
Some signs it is likely include:
 Constant acid reflux
 Burning sensations near chest
bone
 Pain in throat and chest when
eating
 frequent and longstanding heartburn
 trouble swallowing (dysphagia)
 vomiting blood (hematemesis)
 pain under the breastbone where the esophagus meets
the stomach
 unintentional weight loss because eating is painful
Risk factors for development
of Barrett’s esophagus
 Male gender 3 times > female gender
 White race >> Blacks & Asians
 Abdominal adiposity (obesity)
 Genetic factors suspected in some patients/families
 Chronic reflux symptoms for > 5-10 years
 Age >40-50 years; mean age at diagnosis = 55 yrs
Mechanism
 Barrett esophagus occurs due to chronic
inflammation. The principal cause of the chronic
inflammation is gastroesophageal reflux disease,
GERD . In this disease, acidic stomach, bile, small
intestine and pancreatic contents cause damage to the
cells of the lower esophagus
Damage to the squamous
esophageal mucosa
Injury heals
through a metaplastic process
(columnar cells replace squamous cells)
Pathogenesis of Barrett’s Esophagus
GERD
Injury heals
with restoration of
squamous mucosa
Long-segment versus
short-segment Barrett’s esophagus
 Long-segment BE (LSBE): >3-cm segment of distal esophagus (columnar
mucosa with intestinal metaplasia)
 Short-segment BE (SSBE): <3-cm segment (usually tongues or islands of
columnar mucosa with intestinal metaplasia)
 Patients with LSBE tend to have greater esophageal acid exposure than
SSBE, as well as lower LES pressures and more esophageal dysmotility.
 LSBE (classic BE) is much better studied.
 We are currently managing LSBE and SSBE similarly.
 However, questions remain:
 Does SSBE have the same pathogenesis?
 Does SSBE have a lower risk of cancer?
 Does SSBE progress to LSBE?
 Does the length of BE correlate with cancer risk?
Long segement type
Short segement type
Physiology of Barrett’s
Esophagus
 When food becomes backed
up, the juices of the stomach
go back up the esophagus.
 This is also known as severe
acid reflux.
 When having a repeated
injury to the Esophagus
, acidic fluid changes the
types of cells lining it from
squamous to columnar
.(METAPLASIA)
 Fluid may contain bile acids.
Development of Neoplasia in Barrett’s
Esophagus
1
2Gastric acid reflux
2
1Duodenal bile reflux
Pro-carcinogenic
primary and
secondary bile salts
3
pH dependent,bile
salt induced chronic
esophageal injury
4
Chronic esophageal
inflammation and
PGE2release
5
Neoplasia in Barrett’s
esophagus
Development of esophageal adenocarcinoma from
Barrett’s esophagus
 Compelling evidence exists for a dysplasia-carcinoma
sequence in BE.
 Specialized columnar epithelium progresses in some patients
→ low-grade dysplasia → high-grade dysplasia →
adenocarcinoma.
 Not every patient with low-grade dysplasia progresses, and
low-grade dysplasia can even spontaneously revert back to
no dysplasia.
 Time course for development of cancer highly variable.
 Most patients never progress to dysplasia. Less than 5% of
Barrett’s patients will develop cancer.
Why do we care about Barrett’s esophagus?
 Patients with BE have an increased risk of developing esophageal
adenocarcinoma.
 Over the past 30 years, the incidence of squamous cell cancer of the
esophagus has stayed constant, while the incidence of adenocarcinoma
has increased 6-fold! This is an increase that exceeds that of any other
cancer.
 Today, adenocarcinoma accounts for more than half of esophageal
cancers.
 Patients with BE have about a 30-40 fold increased risk of
adenocarcinoma of esophagus.
 Risk of a BE patient developing cancer is estimated to be about 1 per
200 patient-years follow-up.
 Despite all this, most patients with BE do not develop esophageal
cancer. [Less than 5%]
Diagnosis
 GERD is a precursor to the
diagnosis of Barrett’s
Esophagus.
 The tissue lining of the
esophagus has changed.
 Endoscopy (a long thin tube
that examines the lining of
the esophagus and stomach)
confirms whether or not cells
are abnormal.
1. Locate gastro-
esophageal
junction
3. Describe extent of
metaplasia
consistently
2. Recognize the
squamocolumnar
junction
Three Essential Steps for
Endoscopic Diagnosis and
Description
Therapy of Barrett’s Esophagus
Antisecretory therapy
Surgery
Ablation
Chemoprevention
TREATMENT AND
MANAGEMENT TACTICS
 TREATMENT OF the mai cause that is GERD-
Treatment should improve acid reflux symptoms, and
may keep Barrett's esophagus from getting worse.
Treatment may involve lifestyle changes and
medications such as:
 Antacids after meals and at bedtime
 Histamine H2 receptor blockers(viz rantidine
famotidine etc)
 Proton pump inhibitors(pantoprazole,lansoprazole
etc)
N.B.- Lifestyle changes, medications, and anti-
reflux
surgery may help with symptoms of GERD, but will
not
make Barrett's esophagus go away.
TREATMENT OF BARRETT'S ESOPHAGUS
 Surgery or other procedures may be recommended if a
biopsy shows cell changes that are very likely to lead to
cancer. Such changes are called severe or high-grade
dysplasia.
 Surgery
 Removal of intestinal
cells from esophagus and
replacement of
esophageal cells
 Removal of the
esophagus
Recent advance in surgical
method
 Photodynamic therapy (PDT) uses a special laser
device, called an esophageal balloon, along with a drug
called Photofrin.
 Other procedures use different types of high energy to
destroy the precancerous tissue.
 Surgery removes the abnormal lining.
Fun and Interesting Facts
 Only about 1% of all Americans suffer from Barret’s
Esophagus
 10% to 15% of people with chronic GERD get Barrett’s
Esophagus.
 About 3.3 million adults over 50 years of age in the United
States have Barrett’s Esophagus.
 Men are more likely to develop Barrett’s Esophagus than
women and the ratio is 2:1, and EUROPEAN males are
more likely to have it than any other race.
?QUESTIONS?

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  • 2. What is Barrett’s Esophagus?  The esophagus gets a tissue lining similar to that of the intestines  The muscle becomes rougher  The cells that are normally found in the intestine replace the normal esophagus cells
  • 3. Estimated prevalence of Barrett’s esophagus  6-12% of patients who undergo EGD for GERD. Short-segment BE: 6-12% Long-segment BE: 1-5%  1-2% of unselected patients who undergo EGD  Most cases go undetected in the general population [Autopsy data]. Perhaps 5% of patients with Barret esophagus are currently being diagnosed.
  • 4. Symptoms of Barretts esophagus  There are no specific symptoms, they vary per person Some signs it is likely include:  Constant acid reflux  Burning sensations near chest bone  Pain in throat and chest when eating
  • 5.  frequent and longstanding heartburn  trouble swallowing (dysphagia)  vomiting blood (hematemesis)  pain under the breastbone where the esophagus meets the stomach  unintentional weight loss because eating is painful
  • 6. Risk factors for development of Barrett’s esophagus  Male gender 3 times > female gender  White race >> Blacks & Asians  Abdominal adiposity (obesity)  Genetic factors suspected in some patients/families  Chronic reflux symptoms for > 5-10 years  Age >40-50 years; mean age at diagnosis = 55 yrs
  • 7. Mechanism  Barrett esophagus occurs due to chronic inflammation. The principal cause of the chronic inflammation is gastroesophageal reflux disease, GERD . In this disease, acidic stomach, bile, small intestine and pancreatic contents cause damage to the cells of the lower esophagus
  • 8. Damage to the squamous esophageal mucosa Injury heals through a metaplastic process (columnar cells replace squamous cells) Pathogenesis of Barrett’s Esophagus GERD Injury heals with restoration of squamous mucosa
  • 9. Long-segment versus short-segment Barrett’s esophagus  Long-segment BE (LSBE): >3-cm segment of distal esophagus (columnar mucosa with intestinal metaplasia)  Short-segment BE (SSBE): <3-cm segment (usually tongues or islands of columnar mucosa with intestinal metaplasia)  Patients with LSBE tend to have greater esophageal acid exposure than SSBE, as well as lower LES pressures and more esophageal dysmotility.  LSBE (classic BE) is much better studied.  We are currently managing LSBE and SSBE similarly.  However, questions remain:  Does SSBE have the same pathogenesis?  Does SSBE have a lower risk of cancer?  Does SSBE progress to LSBE?  Does the length of BE correlate with cancer risk?
  • 10. Long segement type Short segement type
  • 11. Physiology of Barrett’s Esophagus  When food becomes backed up, the juices of the stomach go back up the esophagus.  This is also known as severe acid reflux.  When having a repeated injury to the Esophagus , acidic fluid changes the types of cells lining it from squamous to columnar .(METAPLASIA)  Fluid may contain bile acids.
  • 12. Development of Neoplasia in Barrett’s Esophagus 1 2Gastric acid reflux 2 1Duodenal bile reflux Pro-carcinogenic primary and secondary bile salts 3 pH dependent,bile salt induced chronic esophageal injury 4 Chronic esophageal inflammation and PGE2release 5 Neoplasia in Barrett’s esophagus
  • 13. Development of esophageal adenocarcinoma from Barrett’s esophagus  Compelling evidence exists for a dysplasia-carcinoma sequence in BE.  Specialized columnar epithelium progresses in some patients → low-grade dysplasia → high-grade dysplasia → adenocarcinoma.  Not every patient with low-grade dysplasia progresses, and low-grade dysplasia can even spontaneously revert back to no dysplasia.  Time course for development of cancer highly variable.  Most patients never progress to dysplasia. Less than 5% of Barrett’s patients will develop cancer.
  • 14. Why do we care about Barrett’s esophagus?  Patients with BE have an increased risk of developing esophageal adenocarcinoma.  Over the past 30 years, the incidence of squamous cell cancer of the esophagus has stayed constant, while the incidence of adenocarcinoma has increased 6-fold! This is an increase that exceeds that of any other cancer.  Today, adenocarcinoma accounts for more than half of esophageal cancers.  Patients with BE have about a 30-40 fold increased risk of adenocarcinoma of esophagus.  Risk of a BE patient developing cancer is estimated to be about 1 per 200 patient-years follow-up.  Despite all this, most patients with BE do not develop esophageal cancer. [Less than 5%]
  • 15. Diagnosis  GERD is a precursor to the diagnosis of Barrett’s Esophagus.  The tissue lining of the esophagus has changed.  Endoscopy (a long thin tube that examines the lining of the esophagus and stomach) confirms whether or not cells are abnormal.
  • 16. 1. Locate gastro- esophageal junction 3. Describe extent of metaplasia consistently 2. Recognize the squamocolumnar junction Three Essential Steps for Endoscopic Diagnosis and Description
  • 17. Therapy of Barrett’s Esophagus Antisecretory therapy Surgery Ablation Chemoprevention
  • 18. TREATMENT AND MANAGEMENT TACTICS  TREATMENT OF the mai cause that is GERD- Treatment should improve acid reflux symptoms, and may keep Barrett's esophagus from getting worse. Treatment may involve lifestyle changes and medications such as:  Antacids after meals and at bedtime  Histamine H2 receptor blockers(viz rantidine famotidine etc)  Proton pump inhibitors(pantoprazole,lansoprazole etc)
  • 19. N.B.- Lifestyle changes, medications, and anti- reflux surgery may help with symptoms of GERD, but will not make Barrett's esophagus go away.
  • 20. TREATMENT OF BARRETT'S ESOPHAGUS  Surgery or other procedures may be recommended if a biopsy shows cell changes that are very likely to lead to cancer. Such changes are called severe or high-grade dysplasia.
  • 21.  Surgery  Removal of intestinal cells from esophagus and replacement of esophageal cells  Removal of the esophagus
  • 22. Recent advance in surgical method  Photodynamic therapy (PDT) uses a special laser device, called an esophageal balloon, along with a drug called Photofrin.  Other procedures use different types of high energy to destroy the precancerous tissue.  Surgery removes the abnormal lining.
  • 23. Fun and Interesting Facts  Only about 1% of all Americans suffer from Barret’s Esophagus  10% to 15% of people with chronic GERD get Barrett’s Esophagus.  About 3.3 million adults over 50 years of age in the United States have Barrett’s Esophagus.  Men are more likely to develop Barrett’s Esophagus than women and the ratio is 2:1, and EUROPEAN males are more likely to have it than any other race.