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ESOPHAGUS
n = 31
n = 25
% of patients achieving pH normalization
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17
A
FIG. 4 Intraoperative images. (A) Dissection of the tunnel between the posterior vagal nerve and the posterior esophageal wall at the inferior border of
the lower esophageal sphincter (LES). (B) The position of the sizing tool to measure the circumference of the esophagus at the lower border of the LES.
(C) Completed implantation of the LINX device around the lower border of the LES with the clasps connected.
B
C
device. The sizing tool is inserted through the far-lateral placed right
upper quadrant port and then passed through the dissected tunnel
between the posterior vagal nerve and esophageal wall and around
the esophagus (see Fig. 4B). Anterior retraction on the previously
placed Penrose drain simplifies this maneuver. When making the
measurement, the surgeon must not intubate the esophagus or
compress its muscular wall by the measuring device. Two measurements should be taken. If the measurement is between two sizes, the
larger size is selected. The most common size is 14, and smaller sizes
should be used sparingly and with caution. The appropriate size of
device is selected and pulled through the tunnel in a left to right
direction. Again, anterior retraction of the Penrose drain simplifies
this maneuver. The ends of the device are brought anteriorly around
the esophagus, the left end around the Angle of His and the right end
over the gastrohepatic branch of the anterior vagal nerve. The clasps
100%
90%
80%
70%
60%
50%
40%
30%
20%
10%
0%
P = 1.000
23/31
(74%)
Limited focused dissection
18/25
(72%)
Extended dissection
are connected, and the anterior portion of the device is placed in the
trench if present (see Fig. 4C). If the right and left crura appear to
diverge from one another above the crural decussation, one or two
figure-of-8 sutures can be placed to approximate them, provided no
further dissection is required. A small hiatal hernia less than 3cm in
FIG. 5 The degree of dissection necessary to implant the LINX antireflux
device and normalization of esophageal acid exposure. With either dissection (limited focus or extended), the esophageal acid exposure was normalized in more than 70% of patients. The durability of competency with
size can be effectively repaired by this maneuver. The surgical time is
usually less than 1 hour. The patient is discharged the same day or, if
with an extended dissection is unknown.
an afternoon procedure, the next morning. The patient is instructed
to slowly return to a normal diet over the next week and discontinue
the use of acid-suppression medication.
For patients with a hiatal hernia greater than 3 cm, a more
extended and less focused dissection can be done to allow dissection and reduction of the hernia into the abdomen, approximation
of the crura around a 2- to 3-cm length of abdominal esophagus,
and implantation of the LINX device. An extended dissection also
provides a fallback solution when greater exposure is necessary to
implant the LINX device for reasons other than a hiatal hernia. Normalization of esophageal acid exposure is similar in patients after a
limited focus or extended dissection (Fig. 5). Again, when doing an
extended dissection, it is important to approximate the crura around
the esophagus in a manner that maintains 2 to 3cm of esophagus
in the abdominal environment. When this is not done, the ability to
deter the reflux of gastric juice into the esophagus caused by episodes
of increased abdominal environmental pressure is compromised.
recently. The final 5-year results of the US Food and Drug Administration’s approved trial provides a careful analysis of the safety and
effectiveness of the LINX device. The studied population consisted
of 100 adults who had GERD for at least 6 months or longer, were
partially responsive to daily PPIs, and had abnormal esophageal
acid exposure on 24-hour pH testing. The LINX device was placed
using standard laparoscopic techniques. In this study, 85 subjects
were followed for 5 years and evaluated for quality of life (GERDHRQL score), reflux control (postoperative 24-hour pH testing at
1 year), use of PPIs, and side effects. A quality of life questionnaire
was administered at baseline to patients on and off PPIs and after
placement of the LINX device yearly for 5 years. Over the follow-up
period, no device erosions, migrations, or malfunctions occurred.
At baseline, the median GERD-HRQL scores were 27 when patients
LONG-TERM CLINICAL OUTCOMES
OF THE LINX MAGNETIC SPHINCTER
AUGMENTATION DEVICE
Long-term outcomes of patients who had the LINX magnetic sphincter augmentation device implanted for GERD have been reported
were not taking PPIs, 11 when taking PPIs, and decreased to 4 at 5
years after LINX placement (Fig. 6). All patients were taking daily
PPIs at baseline, and this decreased to 15.3% at 5 years (Figs. 7 and 8).
Moderate to severe heartburn occurred in 89% of patients at baseline
but only 11.9% at 5 years (see Fig. 7). Moderate to severe regurgitation occurred in 57% of patients at baseline, but only 1.2% at 5 years
18 NEW APPROACHES TO GASTROESOPHAGEAL REFLUX DISEASE (LINX)
baseline
baseline
30
25
20
15
10
100
<
Percent
Baseline Year 1Year 2Year 4Year 5Year 3
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27
11
5
0
FIG. 6 Median total GERD-HRQL scores measured at baseline without
and with proton pump inhibitors, as compared with 5 years after implantation of the LINX sphincter augmentation device. Higher scores indicate
worse symptoms. P < 0.001 for all comparisons with baseline.
Without
proton-pump
inhibitors at
With
proton-pump
inhibitors at
4
5 yr after
sphincter
augmentation
90
80
70
60
None PRN QD BID
100
90
80
70
60
50
40
30
20
10
0
FIG. 8 The use of PPIs at baseline and yearly throughout the 5 years. PPI
use was categorized as none, as needed (PRN), once a day (QD), and twice
a day (BID) at each yearly visit based on the prior 30 days. Patients who
required BID PPIs decreased from 36% at baseline to 2.4% at 5 years.
50
40
Percent of patients
30
20
10
0
Baseline
FIG. 7 Reflux control of moder-
ate-severe heartburn, moderate-severe regurgitation, PPI dependency,
and dissatisfaction with therapy. P <
0.001 between baseline and yearly
follow-up evaluation out to 5 years
for all comparisons. Of the six
patients who were dissatisfied at 5
years, five reported daily use of PPIs.
Heartburn 89 3.2 5.6 8 9.3 11.9
(N = 100)
57 2.1 1.1 2.3 3.4 1.2Regurgitation
100 9.3 7.8 7.9 8.1 15.3PPI dependence
95 3.2 3.3 3.4 5.8 7.1Dissatisfaction
(see Fig. 7). All patients reported the ability to belch and vomit if
needed. Bothersome dysphagia was present in 5% at baseline and in
6% at 5 years (Fig. 9). Bothersome gas bloat was present in 52% at
baseline and decreased to 8.3% at 5 years (see Fig. 9). No significant
complications occurred. No new safety risks emerged over the 5 years
of follow-up. On the basis of this and other reported studies, LINX is
Year 1
(N = 95)
P
.001 for comparision between baseline and all follow-ups
Year 2
(N = 90)
Year 3
(N = 87)
Year 4
(N = 86)
Year 5
(N = 84)
an effective fundic-sparing, antireflux procedure with minimal side
effects. It is applicable to patients who have a partial response to PPIs,
a desire to be off PPIs, or endoscopic/histologic signs of progression
while on PPI therapy. A hiatal hernia is likely not a contraindication
to the use of the LINX device, but long-term results regarding the
recurrence rate of the hiatal hernia are needed.
100
90
6.0
8.3
2.4
6
2.4Year 5
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80
70
60
50
40
Percent of patients
30
20
10
0
Difficulty
swallowing
Bloating/
gassy
Diarrhea Constipation
ESOPHAGUS
Nausea/
vomiting
19
Baseline 5
FIG. 9 Potential side effects of LINX magnetic sphincter augmentation at 5 years when compared with the same symptoms at baseline. P = 0.739 for diffi-
culty swallowing, P < 0.001for bloating/gassy feeling, P = 0.103 for diarrhea, P = 0.008 for constipation, and P = 0.003 for nausea and vomiting.
52
S u g g e S t e d R e a d i n g S
Ayazi S, Tamhankar A, DeMeester SR, Zehetner J, Wu C, Lipham JC, Hagen JA,
DeMeester TR. The impact of gastric distension on the lower esophageal
sphincter and its exposure to acid gastric juice. Ann Surg. 2010;252:57–62.
Bonavina L, DesMeester T, Fockens P, Dunn D, Saino G, Bona D, Lipham
J, Bemelman W, Ganz RA. Laparoscopic sphincter augmentation device
eliminates reflux symptoms and normalizes esophageal acid exposure—
one and 2 year results of a feasibility trial. Ann Surg. 2010;252:857–862.
Bonavina L, Saino GI, Bona D, Lipham J, Ganz RA, Dunn D, DeMeester T.
Magnetic augmentation of the lower esophageal sphincter: results of a
feasibility clinical trial. J Gastrointest Surg. 2008;12:2133–2140.
Bonavina L, Saino G, Lipham JC, DeMeester TR. LINX reflux management sys-
tem in chronic gastroesophageal reflux: a novel effective technology for restor-
ing the natural barrier to reflux. Therap Adv Gastroenterol. 2013;6:261–268.
DeMeester TR, Peters JH, Bremner CG, Chandrasoma P. Biology of gas-
tro-esophageal reflux disease: pathophysiology relating to medical and
surgical treatment. Annu Rev Med. 1999;50:469–506.
Management of
9
Ganz RA, Edmundowicz SA, Taiganides PA, et al. Long-term outcomes of
patients receiving a magnetic sphincter augmentation device for gastroesophageal reflux. Clin Gastroenterol Hepatol. 2016;14:671–677.
Ganz RA, Gostout CJ, Grudem J, Swanson W, Berg T, DeMeester TR. Use
of magnetic sphincter for the treatment of GERD: a feasibility study.
Gastrointest Endosc. 2008;67:287–294.
Ganz R, Peters JH, Horgan S, Bemelman WA, Dunst CM, Edmundowicz SA,
et al. Esophageal sphincter device for gastroesophageal reflux disease.
NEJM. 2013;368:719–727.
Klaus A, Gadenstaetter M, Muhlmann G, Kirchmayr W, Profanter C, Achem
SR, Wetscher GJ. Selection of patients with gastroesophageal reflux disease for antireflux surgery based on esophageal manometry. Dig Dis Sci.
2003;48:1719–1722.
Malfertheiner P, Nocon M, Vieth M, et al. Evolution of gastro-esophageal
reflux disease over 5 years under routine medical care—the ProGERD
study. Aliment Pharmacol Ther. 2012;35:154–164.
18
12
Barrett’s Esophagus
Stephen R. Broderick, MD, MPHS
DEFINITION OF BARRETT’S ESOPHAGUS
AND TREATMENT OBJECTIVES
Barrett’s esophagus (BE) is defined as metaplastic change of the
epithelial lining of the distal esophagus from normal stratified squamous epithelium to intestinal columnar epithelium containing goblet
cells. The diagnosis of BE must be made endoscopically with a visible
change in the lining of the distal esophagus and biopsy demonstrating columnar epithelium with goblet cells (Fig. 1). BE results from
chronic injury to the esophageal mucosa secondary to long-standing
gastroesophageal reflux disease (GERD). Population-based estimates
of the prevalence of BE range from 0.4% to 2%, with higher rates
(5%–15%) among patients with GERD. BE is the major risk factor
FIG. 1 Intestinal metaplasia with goblet cells (arrows).
20 MANAGEMENT OF BARRETT’S ESOPHAGUS
AB
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for esophageal adenocarcinoma (EAC). Therefore, the objectives of
treatment are to treat the underlying reflux disease, prevent progression of BE, and treat BE with dysplasia before progression to EAC.
CLINICAL EFFECT AND FEATURES OF
BARRETT’S ESOPHAGUS
The primary clinical implication of BE is the risk of progression
to EAC. Rates of EAC in Western populations have been increasing over recent decades, and overall survival remains poor despite
improvements in early diagnosis and treatment. Estimates of risk of
EAC in patients with BE range from 30 to 125 times that of the general population. Progression from BE to EAC generally takes place in
a stepwise manner over time from normal squamous epithelium to
non-dysplastic BE, low-grade dysplasia (LGD), high-grade dysplasia
(HGD), and finally EAC. LGD and HGD are determined by the
degree of distortion in the architecture of dysplastic cells. This distinction can be subtle with a high degree of interobserver variability.
In addition to GERD, a number of other risk factors have been
associated with the development of BE and subsequent EAC. These
include family history, age older than 50 years, male sex, central obesity, white race, presence of hiatal hernia, and tobacco use.
SCREENING AND EVALUATION OF
BARRETT’S ESOPHAGUS
Screening
Given the low background prevalence of BE, routine endoscopic screening is not recommended. Various society guidelines exist supporting
screening in patients with risk factors. The American College of Gastroenterology (ACG) Clinical Guidelines support screening for males
with chronic GERD, defined as symptoms for 5 or more years with at
least weekly symptoms and two or more additional risk factors (age >50,
white race, central obesity, current or past smoking, family history in a
first-degree relative). Screening is not recommended in women but may
be considered on an individual basis if risk factors are present.
Evaluation
The initial evaluation for BE consists of white light endoscopy. BE
should be suspected when salmon pink mucosa is identified proximal to the gastroesophageal junction (GEJ). The endoscopist should
inspect for areas of columnar metaplasia as well as irregularities in
the mucosal surface. These may signify areas of dysplasia or invasive
adenocarcinoma. The Prague classification is the most commonly
used standardized reporting mechanism which identifies the proximal extent of circumferential BE as well as the maximal extent of
any tongues of BE. The presence and size of any hiatal hernia should
also be noted.
Biopsies should be taken of the distal esophagus in four quadrants
from the GEJ at 1- to 2-cm intervals through the proximal extent of
suspected BE (the Seattle protocol). Biopsies of the gastric mucosa
for comparison purposes and of any areas with mucosal irregularity
should also be taken. Narrow band imaging (or another form of
chromoendoscopy) should be employed to enhance visualization
of mucosal surface vascular patterns and irregularities (Fig. 2). The
finding of BE with dysplasia requires confirmation by a second
pathologist with gastrointestinal (GI) expertise.
SURVEILLANCE
Current practice guidelines from both medical and surgical societies
universally recommend endoscopic surveillance once BE is identified. The goal of surveillance is to identify progression to dysplasia or
EAC at an early, treatable stage. There is some degree of variation in
the details of surveillance protocols. Areas of consensus and debate
include the following:
1. White light endoscopy is the preferred method of surveillance
with or without the addition of narrow band imaging.
2. There is near consensus that the Seattle protocol consisting of
four-quadrant biopsies is the optimal biopsy strategy, with some
debate over a 1-cm versus 2-cm interval between biopsies. All
nodular lesions should be biopsied and sent separately for patho-
logic evaluation. Some guidelines recommend against biopsies
in areas of active esophagitis, favoring repeat endoscopy after a
period of suppressive therapy.
3. There is unanimity that dysplasia should be confirmed by a sec-
ond pathologist with expertise in GI pathology.
4. Guidelines are consistent regarding a surveillance interval of 3 to
5 years for nondysplastic BE. There is variation in the impact of
the length of the BE segment on the recommended surveillance
interval, with some guidelines suggesting shorter intervals for
patients with longer-segment BE.
FIG. 2 Barrett’s esophagus seen on endoscopy under both white light endoscopy (A) and narrow band imaging (B).
NBI
ESOPHAGUS
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21
5. There is no consensus regarding when to stop surveillance. Cessation is recommended when patients are no longer candidates
for endoscopic or surgical therapy or cannot tolerate repeat endoscopic procedures.
MANAGEMENT OF BARRETT’S
ESOPHAGUS WITHOUT DYSPLASIA
The overriding principle in managing a patient with non-dysplastic
BE is treatment of underlying GERD. This will accomplish not only
symptom control but also protect the esophageal mucosa from repetitive reflux injury. Medical therapy with once-daily dosing of proton
pump inhibitors (PPIs) is the recommended first-line therapy in
addition to diet and lifestyle modifications. Escalation to twice-daily
dosing is recommended only when symptom control on daily dosing
is inadequate.
Antireflux surgery is an adjunct to medical therapy for GERD.
Data supporting the role of surgery in preventing progression to EAC
are weak. Therefore, surgery is recommended for failure of medical
therapy to control symptoms or impaired quality of life. The role or
benefit of mucosal ablation with radiofrequency or other modalities
is unproven in patients with non-dysplastic BE. There may be a role
for ablation in patients with ultralong segment (>8 cm) BE to reduce
the complexity of biopsy procedures.
Regardless of the approach to treat GERD (medical therapy or
surgery), surveillance endoscopy is necessary to evaluate for progression to dysplasia.
MANAGEMENT OF BARRETT’S
ESOPHAGUS WITH LOW-GRADE
DYSPLASIA
LGD is associated with an increased risk of progression to adenocarcinoma compared with nondysplastic BE. The presence of LGD
on any biopsy necessitates thorough evaluation with four-quadrant
biopsies every 1 to 2 cm over the entire area of BE if not already
performed. The presence of dysplasia should be confirmed by an
expert GI pathologist, as the distinction of LGD from inflammatory
atypia can be subtle. Patients with LGD should then be initiated on
PPI therapy with repeat endoscopic evaluation in 6 months. LGD
will often regress to nondysplastic BE with PPI therapy. Antireflux
surgery should be considered at the identification of LGD or if
LGD persists despite initiation of PPIs. Nissen fundoplication has
demonstrated superior rates of regression of LGD compared with
PPI therapy alone.
Persistent dysplasia despite control of GERD with PPI and/or
antireflux surgery is an indication for mucosal ablation. Radiofrequency ablation has been shown to reduce the risk of progression to
adenocarcinoma compared with surveillance alone.
MANAGEMENT OF BARRETT’S
ESOPHAGUS WITH HIGH-GRADE
DYSPLASIA
Given the proven high risk for progression to EAD, the presence of
BE with HGD is an indication for intervention in most patients. If
initial endoscopic evaluation identifies HGD, a careful repeat endoscopy is performed to thoroughly map areas of HGD and identify
any areas of nodularity or ulceration in the metaplastic columnar
mucosa. Both white light and narrow band imaging (or another form
of chromoendoscopy) should be employed to aid in identification of
mucosal lesions.
Endoscopic mucosal resection (EMR) should be used to remove
any small, discrete nodules. In EMR, a cap is attached to the tip
of the endoscope, the target lesion is suctioned into the cap, and a
band is applied to the base, creating a “pseudopolyp.” This is then
snared and sent for pathologic evaluation. In lesions 1 cm or larger,
endoscopic ultrasound (EUS) is employed to assess for invasion into
the esophageal wall and presence of periesophageal lymphadenopathy. EUS is not useful for very small lesions or HGD in which no
mucosal abnormality is identified. In the event that an EMR specimen demonstrates adenocarcinoma, the depth of invasion (Tis vs.
T1a vs. T1b) is critical in determining the next steps in evaluation
and treatment. Thus, a good EMR specimen will contain mucosa
and submucosa, leaving muscularis at the base of the resection site.
The ER specimen can also be evaluated for other high-risk features
including degree of differentiation or lymphovascular invasion,
which may prompt more aggressive management. Invasion into
the submucosa (T1b), a poorly differentiated lesion, and lymphovascular invasion increase the likelihood of occult lymph node
metastases. Thus, these features should prompt further staging
investigations and consideration of esophagectomy in appropriate
surgical candidates.
Patients found to have HGD alone or adenocarcinoma confined
to the mucosa (T1a) without high-risk features are candidates for
endoscopic interventions to ablate the lesion(s) and preserve the
esophagus. The goal of endoscopic therapy should be resection of
all raised or suspicious mucosal lesions. This can be accomplished
with in one or multiple sessions over a 6- to 8-week period until all
documented areas of dysplasia are removed. Oftentimes ablation of
the residual metaplastic mucosa is then performed to reduce the risk
of progression to further areas of dysplasia.
After complete eradication of both dysplasia and intestinal metaplasia, ongoing surveillance is essential. Surveillance endoscopy after
ablation of HGD should be performed every 3 months for the first
year, every 6 months for the second year, and annually thereafter if
no recurrent areas of dysplasia are identified. It is also critical that
patients with documented HGD achieve long-term control of underlying GERD with medical therapy or antireflux surgery.
Esophagectomy in High-Grade Dysplasia
Although endoscopic therapies are now the standard of care, there
remains a role for esophagectomy in select patients in whom BE with
HDG is identified. Esophagectomy provides the most thorough eradication of the diseased esophagus but carries the significant potential
morbidity and mortality of surgery. Operative mortality associated
with esophagectomy for HGD is less than 1% at experienced centers. Esophagectomy is considered in patients with the following
characteristics:
■ High-risk features: length > 2 to 3 cm, lymphovascular invasion,
multifocality, poorly differentiated lesion
■ Patient with preference for surgery or inability to attend repeat
surveillance or procedural endoscopies
■ Inability to eradicate areas of HGD with endoscopic therapies
■ Evidence of progression despite endoscopic ablation
■ Technically insufficient endoscopic ablation
■ End-stage esophageal function (secondary to motility disorder,
stricture, hernia)
CONSIDERATIONS REGARDING
ANTIREFLUX SURGERY IN BARRETT’S
ESOPHAGUS
GERD that leads to BE is associated with a higher degree of reflux,
incompetent lower esophageal sphincter (LES), esophageal dysmotility, and hiatal hernia. These factors lead to lower likelihood of control
of GERD with medical therapy alone. Antireflux surgery has several
theoretical benefits in the management of GERD, including the control of both acid and biliopancreatic substrates that are contributing
to mucosal injury and restoration of the hiatus and incompetent LES.
More complete control of reflux into the distal esophagus has been
22 MANAGEMENT OF BARRETT’S ESOPHAGUS
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associated with more frequent regression of BE and reduced rates of
progression to EAC.
Antireflux surgery in the setting of esophageal dysmotility or
hiatal hernia can be more challenging than routine fundoplication. Fundoplication is more likely to fail in patients with BE, and
failure is associated with progression of BE. Thus, patients who
undergo antireflux procedures still require frequent surveillance
endoscopy.
In addition to endoscopy, evaluation of the patient with BE for
consideration of antireflux surgery consists of contrast esophagram
and high-resolution manometry. Preoperative and postoperative
pH testing can assist in determining which patients can discontinue
PPI therapy following fundoplication. Consideration to the type of
fundoplication (complete vs. partial) should be given based on the
patient’s esophageal motility.
Chronic GERD symptoms (>5 years) and ≥2 risk
factors for esophageal adenocarcinoma (age ≥50 y,
male, white, elevated BMI, smoking history)
Screening endoscopy
Diagnosis of BE
(Confirmed with EGD and biopsy)
CONCLUSION
Management of the patient with BE is closely associated with management of the patient’s underlying GERD. There are two intertwined
objectives of therapy: (1) identification, treatment, and surveillance of
intestinal metaplasia and (2) treatment of the underlying GERD. Combined, these strategies serve to reduce the risk of progression from nondysplastic BE to dysplasia or adenocarcinoma. In addition, treatment
of GERD reduces symptomatology and improves dietary quality of life.
Antireflux surgery can be beneficial to eradicate GERD symptoms,
induce regression of dysplasia, and reduce the chance of progression.
Patients should be carefully selected for surgery as those with BE are
commonly associated with hiatal hernia and esophageal dysmotility,
putting them at higher risk for failure of fundoplication. Endoscopic
therapies are now the standard of care for patients with dysplasia and
Incidental finding of BE on
endoscopy performed for
other reasons
No dysplasia
Consider repeat
EGD with
biopsy within
1 year of initial
diagnosis
No dysplasia
Repeat EGD
and biopsy every
3-5 years
(consider
1-3 years based
on risk)
No dysplasia
Annual
surveillance for
2 years
Follow protocol
for no dysplasia
Control GERD
with PPI
Low-grade dysplasia
Repeat EGD
with biopsy in
3-6 months
Confirmed low-
grade dysplasia
Consider
endoscopic
ablation versus
surveillance
every 6-12
months
High-grade dysplasia
(HGD)
Follow HGD
algorithm
Progression
to HGD
Follow HGD
algorithm
FIG. 3 Management of Barrett’s esophagus. BE, Barrett’s esophagus; BMI, body mass index; EGD, esophagogastroduodenoscopy; GERD, gastroesophageal
reflux; PPI, proton pump inhibitor.
Long-term GERD management with PPI or antireflux surgery is mandatory
Long-
High-grade dysplasia (HGD) or
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suspected intramucosal cancer (IMC)
ESOPHAGUS
23
No visible
lesion
Endoscopic
ablation (every
8 weeks) until
eradication
Repeat EGD with
biopsy every 3
months for 1 year,
then every 6 months
for 1 year, then
annually thereafter
Long-term GERD management
with PPI or antireflux surgery
*Reasons to consider
esophagectomy in biopsy proven HGD:
Poor prognostic risk factors of the lesion:
large size (>2-3 cm), lymphovascular
invasion, multifocality
Patient prefers surgery
Unable to comply with the repeat
endoscopic treatments and surveillance
Inability to eradicate HGD and/or
adenocarcinoma or progression of disease
Failed ablation techniques
End-stage esophageal function (due to
motility disorder, stricture, obstructed
hiatal hernia)
Esophagectomy*
Multidisciplinary
discussion
recommended
HGD/stage T1a
Endoscopic
ablation for
residual
metaplastic
disease (every 8
weeks)
Repeat EGD
with biopsy
every 3 months
and annually
thereafter
Long-term GERD
management with PPI
or antireflux surgery
Visible lesion
Endoscopic
resection
for removal and
staging
Esophagectomy*
Stage T1b
Esophagectomy
with
lymphadenectomy
FIG. 4 Management of high-grade dysplasia and intramucosal cancer (IMC). EGD, Esophagogastroduodenoscopy; GERD, gastroesophageal reflux; PPI, proton
pump inhibitor.
allow for preservation of the esophagus. However, there remains a role
for esophagectomy in select patients with BE (Figs. 3 and 4).
S u g g e S t e d R e a d i n g S
Johnson CS, Louie BE, Wille A, et al. The durability of endoscopic therapy
for treatment of Barrett’s metaplasia, dysplasia, and mucosal cancer after
Nissen fundoplication. J Gastrointest Surg. 2015;19(5):799–805.
Maret-Ouda J, Konings P, Lagergren J, Busselaers N. Antireflux surgery and
risk of esophageal adenocarcinoma: a systematic review and meta-analysis. Ann Surg. 2016;263(2):251–257.
Oelschlager BL, Barreca M, Chang L, Oleynikov D, Pellegrini CA. Clinical
and pathologic response of Barrett’s esophagus to laparoscopic antireflux
surgery. Ann Surg. 2003;238(4):458–464.
Parasa S, Vennalaganti S, Gaddam S, etal. Development and validation of a
model to determine risk of progression of Barrett’s esophagus to neoplasia. Gastroenterology. 2018;154(5):1282–1289.
Shaheen NJ, Falk GW, Iyer PG, Gerson LB. ACG Clinical guideline diag-
nosis and management of Barrett’s esophagus. Am J Gastroenterol.
2016;111(1):30–50.
24 ENDOSCOPIC TREATMENT OF BARRETT’S ESOPHAGUS
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Endoscopic Treatment
of Barrett’s Esophagus
Anne P. Ehlers, MD, MPH, and Brant K. Oelschlager, MD
arrett’s esophagus (BE) is a disease characterized by the gradual
replacement of the normal stratified squamous epithelium of
B
the esophagus with columnar, intestinal metaplasia (Figs. 1 and 2).
This transformation is due to chronic exposure to gastric contents,
often within the context of gastroesophageal reflux disease (GERD).
Patients at risk for BE are screened with endoscopy and biopsy. The
major concern with BE is that it is a precursor lesion for esophageal
adenocarcinoma (EAC), a disease with poor prognosis and poor
long-term survival. In addition, EAC is a disease that continues to
increase in incidence. Given this, identifying and eradicating BE
before progression to adenocarcinoma is a top priority. In the past,
patients with BE often were recommended for esophagectomy. More
recently, evolving endoscopic techniques have replaced esophagectomy for many of these patients, allowing for eradication of BE with
less morbidity and fewer complications.
SURVEILLANCE AND MANAGEMENT
ALGORITHM
Screening
The primary risk factor for BE is longstanding GERD, along with
male sex, age older than 50 years, and central obesity. Patients with
GERD have a 10% to 15% risk of BE; increasing age and long-segment BE (>3 cm) are risk factors for progression to dysplasia. Overall, the rate of progression from BE to esophageal adenocarcinoma is
low, perhaps as low as 0.12% per year. Other evidence suggests that
for patients with nondysplastic BE, the annual risk of progression to
EAC is 0.33% per year among all patients with BE and 0.19% per year
among patients with short-segment BE (<3 cm). For patients with
low-grade dysplasia (LGD), this risk increases to 0.5% per year. The
risk increases substantially among those with high-grade dysplasia
(HGD), up to 19% in some studies. Early detection of invasive cancer
is important because patients detected at an early stage have a much
higher 5-year survival rate (83%–90%) compared with patients who
present symptomatically with more advanced disease (10%–30%).
Identifying the most appropriate pool of patients for screening is
an area of active debate, especially with the large number of adults
who have GERD. Because only a minority of patients with GERD
will ever develop BE, screening every patient with GERD is neither
feasible nor efficient. However, evidence suggests that surveillance of
BE is associated with diagnosis of EAC at an earlier stage, which may
be associated with improved outcomes. For these reasons, accurately
identifying the population of patients with BE is critical. Current
guidelines from the American College of Gastroenterology (ACG)
recommend screening male patients with 5 or more years of GERD
symptoms AND two or more risk factors for BE or EAC (age >50
years, white race, central obesity, history of smoking, family history
of BE or EAC). Screening for female patients is generally not recommended, except for patients with multiple risk factors, as outlined
previously.
Screening is generally undertaken using high-resolution endoscopy with liberal use of narrow band imaging and biopsy, but as
previously stated this can be very labor and time intensive. Several
novel screening modalities have been proposed to reduce this
burden. One alternative is transnasal esophagoscopy, which is an
office-based procedure that uses topical anesthetic to pass an endoscope through the nares and into the esophagus. Compared with
traditional high-resolution endoscopy, the image quality is reduced
and the biopsies are smaller but often are sufficient for histologic
analysis to allow a diagnosis of BE to be made without a formal
endoscopy. A second option for screening is the Cytosponge, which
is a gelatin-coated capsule attached to a string that is then swallowed
by the patient. Once in the stomach, the gelatin coating dissolves
leaving behind a sponge that is then retrieved by pulling on the
string. As the sponge comes back through the esophagus, it picks up
cells that can then be examined for abnormalities. It currently holds
promise as a screening tool for BE but is not adequate to screen for
EAC. Because transnasal esophagoscopy and Cytosponge are still
relatively new, high-resolution endoscopy is still the gold standard
for diagnosis of BE.
Surveillance
Patients with confirmed BE in the absence of dysplasia or EAC
should be regularly surveilled to detect disease progression. A challenge in the past has been lack of universal criteria for describing
the extent of disease. To address this challenge, the Prague Criteria
are a set of endoscopic data developed and validated by a working
group specifically focused on esophagitis using standardized videos
of endoscopies. The purpose was to improve on the previously used
vague descriptions of “long” versus “short” segment disease and to
facilitate communication between providers. The Prague Criteria
measures the extent of disease based on circumference and maximum extent (C&M) criteria, with C being the maximum circumferential extent of disease and M the maximum length, including any
isolated tongues of disease.
Once a patient has been diagnosed with BE, the next step is to
evaluate for any dysplasia or invasive cancer. The current recommendation is to evaluate the patient with high-resolution or high-definition white light endoscopy followed by meticulous inspection of the
esophageal lumen, after both insufflation and desufflation, including
inspection of the gastroesophageal junction in the retroflexed view.
Some data suggest that longer inspection time is associated with
better detection of dysplasia or EAC. Suspicious lesions such as erosions, ulcerations, nodules, plaques, and other mucosal or luminal
abnormalities should be selectively sampled. Random biopsies are
not recommended. Suspicious lesions in patients with known dysplasia are best removed via endoscopic mucosal resection (EMR), which
will be described later in the chapter. Additionally, the ACG recommends against taking biopsies in areas of active, erosive esophagitis
and instead suggests waiting until the patient has been treated with
antisecretory agents to allow the inflammation to subside.
Ongoing surveillance is dependent on the pathology determined
at the time of biopsy. For patients who have BE without evidence of
dysplasia, the recommendation is that they undergo repeat endoscopic surveillance every 3 to 5 years, as described previously. In
cases in which biopsies are inconclusive for dysplasia, patients should
be placed on an acid suppression regimen for 3 to 6 months, after
which repeat endoscopy should be performed. If the biopsies are still
inconclusive at that time, repeat endoscopy should be performed 12
months later. If dysplasia is diagnosed (LGD or HGD), the biopsies
should be reviewed by two separate pathologists, one of whom is an
expert in gastrointestinal pathology because there is a high level of
interobserver variability when it comes to dysplasia.
Once dysplasia is confirmed, the next steps depend on the degree
of dysplasia. For LGD, endoscopic therapy is preferred for patients
without significant comorbidity; however, repeat endoscopy in 12
months is acceptable in these cases. For HGD, endoscopic therapy is
recommended except in the case of life-limiting comorbid conditions.
Patients with a diagnosed cancer should undergo further staging
workup to determine whether the cancer is resectable, and some early
adenocarcinomas can be managed endoscopically. For certain young
patients with long-segment multifocal HGD, recurrent HGD, or
ESOPHAGUS
AB
CD
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25
FIG. 1 Spectrum of dysplasia grading. (A) Negative for dysplasia. Although some nuclear hyperchromasia is noted, it is limited to the normal proliferative
zone with evidence of surface maturation. (B) Low-grade dysplasia shows basally oriented, hyperchromatic nuclei with pseudostratification. Crypt architecture is preserved. (C) High-grade dysplasia demonstrates prominent mitotic activity, enlarged nuclei, and loss of nuclear polarity with evidence of glandular
crowding. (D) This lesion shows cytoarchitectural atypia, equivalent to that of low-grade dysplasia, in the deep glands. However, given the presence of surface maturation and the stromal changes suggestive of a reparative process, it is best classified as indefinite for dysplasia. (From Hagen CE, Lauwers GY, Mino-
Kenudson M. Barrett esophagus: diagnostic challenges. Semin Diagn Pathol. 2014;32:100–113.)
intramucosal cancer, surgery should be considered. Asummary of the
surveillance and treatment algorithm is provided in Figures 3 and 4.
PRINCIPLES OF ENDOSCOPIC
THERAPIES
The current evidence suggests that endoscopic therapy should
be used for patients with BE who have LGD, HGD, and for some
patients with early intramucosal (T1a) EAC because the risk of
lymph node metastasis is nonexistent for LGD and HGD and is
removing it before development of invasive disease or destroying
abnormal tissue (ablative techniques). The intestinal metaplasia is
then replaced with normal appearing squamous epithelium (Fig. 5).
ENDOSCOPIC RESECTION TECHNIQUES
Endoscopic Mucosal Resection
EMR is a technique that allows removal of lesions within segments
of BE for complete histologic analysis, including dysplasia and
superficial T1a adenocarcinoma. It offers an advantage over ablative
techniques because it allows for examination of tissue specimens,
initial treatment modality for patients with nodular BE. For patients
26 ENDOSCOPIC TREATMENT OF BARRETT’S ESOPHAGUS
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without high-risk features (submucosal invasion, poor differentiation, or lymphatic vascular invasion), EMR has 98.8% eradication
rate of BE; in patients with high-risk features, the rate is 80.6%. For
T1a tumors, EMR has a 91% to 98% eradication rate.
method, the endoscope is fitted with a transparent cap. Once located,
the target lesion is sucked into the cap and a specialized electrocautery snare is used to resect the lesion. A submucosal injection can be
performed to facilitate this. In the ligation-assisted method, lesions
are removed using a band-ligation device attached to the tip of the
endoscope. Once identified, the target lesion is again sucked into the
endoscope and the band is applied around the lesion to create a pseudopolyp. Electrocautery is then used to remove the pseudopolyp. In
the injection-assisted technique, the submucosal space is injected to
lift the lesion and allow it to be snared and cut.
which occurs in up to 40% of patients. Typically, these lesions can
be managed with endoscopic dilation or stents. EMR is often used in
conjunction with radiofrequency ablation (RFA) with good effect. In
a recent systematic review, EMR alone had a 33.5% risk of stricture,
7.5% risk of bleeding, and 1.3% risk of perforation compared with
10.2%, 1.1%, and 0.2%, respectively, in patients undergoing EMR in
FIG. 2 Endoscopic image of Barrett’s esophagus. The arrows mark the
esophagogastric junction, which is identified endoscopically as the most
proximal extent of the gastric folds. The reddish color and velvet-like texture
of the Barrett’s epithelium contrast sharply with the pale and glossy appearance of the esophageal squamous epithelium. Note that the Barrett’s columnar epithelium extends well above the esophagogastric junction to line the
distal esophagus. (From Spechler SJ, Souza RF. Barrett’s esophagus. In: Sleisenger
and Fordtran’s gastrointestinal and liver disease. Philadelphia: Elsevier; 2016.)
conjunction with RFA.
Endoscopic Submucosal Dissection
Endoscopic submucosal dissection (ESD) is a technique that allows
for complete, en bloc resection of suspicious lesions to allow for
thorough histologic evaluation. When compared with EMR, it also
There are several methods used for EMR. In the cap-assisted
One of the primary side effects of EMR is esophageal stricture,
Flat columnar
mucosa
Systematic
cold biopsy
Nondysplastic
BE
Repeat EGD w/
biopsies in 3–5
years
Confirmed
EGD w/
biopsies in 1
FIG. 3 Management of nonnodular Barrett’s esophagus (BE). *Although endoscopic eradication therapy is associated with a decreased rate of progression,
surveillance upper endoscopy at 1-year intervals is an acceptable alternative. This algorithm assumes that the T1a esophageal adenocarcinoma (EAC) displays
favorable characteristics for endoscopic therapy, including well-differentiated histology and lack of lymphovascular invasion. HGD, High-grade dysplasia; LGD,
low-grade dysplasia; PPI, proton pump inhibitor. (From Shaheen NJ, Falk GW, Iyer PG, etal. ACG Clinical Guideline: Diagnosis and Management of Barrett’s Esophagus.
Am J Gastroenterol. 2016;111:30–51.)
year
Indefinite for
dysplasia
Optimize PPI
therapy
repeat EGD
new histology
Confirmed LGD
Discordant
Manage per
Endoscopic
eradication
therapy
*
Confirmed
HGD
Endoscopic
eradication
therapy
T1a EAC
Endoscopic
eradication
therapy
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