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194
as necessary to gain adequate exposure for lesions located more proximally. To help
exposing the entire lesion, a Penrose drain may be used to encircle the esophagus for
retraction. In the case of leiomyoma, a longitudinal myotomy is performed over the
tumor, which appears as a smooth gray-white mass. Dissection of the tumor from the
muscle and submucosa can be done by using hook electrocautery or scissors. A
retraction suture may be placed through the tumor to assist in this step. Dissection of
other benign intramural tumors can also be performed in the same fashion.
In the case of large infl ammatory cysts, decompression under direct vision of the
cyst can be performed before mobilization [ 45 ]. Then, dissection is performed,
using hook electrocautery, ultrasonic shears, or scissors.
The specimen is put in a bag and removed through a port site. Continuity of the
mucosa must be confi rmed by direct inspection with air insuffl ation through an
endoscope. If there is a mucosal injury, it is repaired using interrupted absorbable
stitches. The muscular defect is closed with absorbable sutures to prevent the poten-
tial development of a pseudodiverticulum [ 55 , 56 ]. Care must be taken not to nar-
row the esophageal lumen. If the muscle closure is not secure, a fl ap of pleura,
pericardium, diaphragm, or pedicled intercostal muscle may be used as a buttress
for the closure. A pleural drain is placed and the port sites are closed while the lung
is reexpanded. A nasogastric tube is not required. A clear liquid diet can be started
on the day of surgery and gradually advanced to a soft diet for patients who do not
have any mucosal perforation. In patients who require mucosal repair, liquid feed-
ings are delayed for 1–2 days to ensure integrity of the closure. Routine postopera-
tive imaging of the esophagus is not required.
Laparoscopic Enucleation
This procedure is indicated for patients who have a benign intramural tumor at or
near the gastroesophageal junction [ 3 , 14 , 57 , 58 ]. Some authors apply this approach
for tumors as high as the distal third of the esophagus [ 59 , 60 ]. The patient is placed
supine or in a modifi ed lithotomy position, under standard general anesthesia. An
endoscopy may be performed to confi rm the site of the lesion. The surgeon stands
at the right side of the patient or between the patient’s legs. A pneumoperitoneum is
created and ports are placed. Generally, 5 ports are used (Fig. 14.2 ): a camera port,
three working/retraction ports, and a port for the liver retractor. The hiatus is opened
and the esophagus is dissected suffi ciently to expose the tumor. Intraoperative
endoscopy may be used for small or deep tumors to identify the margins. Enucleation
is performed as described above using hook electrocautery, scissors, or a sealing
device. Care should be taken to avoid injury to the mucosa and vagal nerves. The
mass is removed and the air-leak test is performed using an endoscope. The muscu-
lar edges are closed over the defect with interrupted sutures. The crura of the dia-
phragm are also approximated using interrupted stitches. No drain is left. In cases
of preexisting gastroesophageal refl ux, a fundoplication should be performed.
Postoperative care is the same as for thoracoscopic enucleation.
P. Hiranyatheb and M.K. Ferguson
195
Minimally Invasive Gastroesophageal Resection
Partial resection of a gastroesophageal segment via minimally invasive tech-
niques is indicated in large tumors or those with circumferential involvement as
described above. Preoperative preparation and positioning are similar to those
for thoracoscopic enucleation. The extent of the resection and the location of the
anastomosis depend on the site of the tumor; the anastomosis can be done in the
chest in case of lower esophageal tumors, whereas a cervical anastomosis is
usually required for upper thoracic tumors. There are 3 minimally invasive sur-
gical options similar to those for esophageal cancer including Ivor-Lewis resec-
tion, the 3-hole (or McKeown) approach, and laparoscopic transhiatal
esophagectomy.
Outcomes and Complications
The outcomes and complications of thoracoscopic and laparoscopic benign tumor
resection are summarized in Tables 14.3 and 14.4 . The results are excellent with
minimal complications, very low mortality, and no tumor recurrence in the reports.
When compared to an open-thoracotomy approach, some specifi c potential compli-
cations, such as pseudodiverticulum and GERD, may be of concern because of a
reduction of propulsive activity and acid-clearing ability after myotomy [ 12 ].
Although there is no strong evidence to support this, most authors still repair the
muscular defect to prevent those potential problems. The outcomes of thoracoscopic
•
•
•
•
•
Liver retractor
Camera port
Retraction
port
Fig. 14.2 Positions of the
ports and liver retractor for
laparoscopic resection of
benign esophageal tumors
14 Minimally Invasive Treatment of Benign Esophageal Tumors
196
esophageal cyst removal are also good, with low rates of complications and very
low mortality [ 45 , 46 , 51 , 52 ]. However, the number of patients in each report is
very small. More studies are needed to clearly demonstrate the effi cacy and safety
of minimally invasive approaches for these lesions.
Conclusions
Benign tumors of the esophagus are rare and are usually asymptomatic. Some of
them can give rise to important problems. The results of small case series indicate
that various methods of endoscopic and minimally invasive surgery for manage-
ment of these problems are feasible, effi cacious, and safe. Most small intraluminal
lesions can be removed endoscopically, whereas minimally invasive procedures are
optimal for leiomyomas and other intramural tumors, having the advantage of
avoiding open surgery. Proper patient selection as well as experienced physicians is
required for good outcomes.
Table 14.3 Outcomes of thoracoscopic enucleation
Authors Year n
Tumor size [cm]
Morbidity
Note Average Range n [%]
Roviaro et al. [
59 ] 1998 6 NR NR
Zaninotto et al. [
57 ] 2006 7 4.3 3–5 0 [0]
Kent et al. [
14 ] 2007 9 3.5 0.9–8 (laparoscopy
included)
2 [22] Pneumonia 1
GERD 1
von Rahden et al. [
54 ] 2008 10 3.5 0.5–5 0 [0]
Palanivelu et al. [
17 ] 2008 6 6.3 4.6–7 2 [33] Pneumonia
Subcutaneous
emphysema
Luh et al. [
15 ] 2012 12 5.0 1–8 0 [0]
Note: GERD gastroesophageal refl ux, n number of patients, NR not reported
Table 14.4 Outcomes of laparoscopic enucleation
Authors Year n
Tumor size [cm] Morbidity
Note Average Range n [%]
Zaninotto et al. [
57 ] 2006 4 4.8 2–5 1 [25] Esophageal
perforation 1
Kent et al. [
14 ] 2007 7 3.5 0.9–8 {thoracoscopy 2 [22] Arrhythmia 1
GERD 1
von Rahden et al. [
54 ] 2008 3 2.0 0.5–4 0 [0]
Palanivelu et al. [
17 ] 2008 7 6.6 5.0–7 1 [14] Bowel ileus
Nguyen et al. [
3 ] 2008 1 1.1 – 0 [0]
P. Hiranyatheb and M.K. Ferguson
197
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14 Minimally Invasive Treatment of Benign Esophageal Tumors
201
P.M. Fisichella et al. (eds.), Surgical Management of Benign Esophageal Disorders,
DOI 10.1007/978-1-4471-5484-6_15, © Springer-Verlag London 2014
Abstract Barrett’s esophagus (BE) involves specialized intestinal metaplasia of
the esophagus and is a precursor of esophageal adenocarcinoma. Although no ran-
domized trials have demonstrated mortality benefi t, we recommend patients with
multiple risk factors for BE undergo endoscopic screening for dysplasia (which
should be confi rmed by an expert pathologist). Patients with BE should be treated
with proton pump inhibitor (PPI) and be considered for PPI even in the absence of
refl ux symptoms or refl ux esophagitis. We recommend patients with BE with no
dysplasia, low-grade dysplasia (LGD), and high-grade dysplasia (HGD) (in the
absence of eradication therapy) have endoscopic surveillance. In most patients with
BE-associated HGD, we recommend endoscopic eradication therapy rather than
surgery or intensive surveillance. This involves endoscopic mucosal resection
(EMR) for removal and staging of visible lesions (if present) followed by radiofre-
quency ablation or photodynamic therapy to ablate remaining metaplastic epithe-
lium. Surgery is a reasonable alternative in young patients with HGD and
long-segment BE or multifocal dysplasia, whereas intensive surveillance is reason-
able in elderly and frail patients where endoscopic therapy might pose a substantial
risk.
Keywords Barrett’s esophagus • Esophageal adenocarcinoma • Endoscopic
mucosal resection • Radiofrequency ablation • Gastroesophageal refl ux disease •
Dysplasia surveillance
Chapter 15
Barrett’s Esophagus: Treatment Options
and Management
Wesley D. Leung and Irving Waxman
W. D. Leung , MD • I. Waxman , MD, FASGE (*)
Section of Gastroenterology, Center for Endoscopic Research and Therapeutics (CERT) ,
University of Chicago Medical Center , Chicago , IL , USA
e-mail: Wesley_leung6@hotmail.com; iwaxman@medicine.bsd.uchicago.edu
202
Abbreviations
APC Argon plasma coagulation
BE Barrett’s esophagus
EAC Esophageal adenocarcinoma
EMR Endoscopic mucosal resection
ESD Endoscopic submucosal dissection
EUS Endoscopic ultrasound
GERD Gastroesophageal refl ux disease
HGD High-grade dysplasia
IGD Indeterminate-grade dysplasia
IMC Intramucosal carcinoma
LGD Low-grade dysplasia
NDBE Non-dysplastic Barrett’s esophagus
PDT Photodynamic therapy
PPI Proton pump inhibitor
RFA Radiofrequency ablation
Introduction
Barrett’s esophagus (BE) is a condition characterized by specialized intestinal meta-
plasia of the esophagus and is recognized as the only known precursor lesion to
esophageal adenocarcinoma (EAC). The development of BE is thought to be a
reparative response to chronic refl ux injury to the squamous esophageal epithelium,
resulting in metaplasia to intestinal epithelium. BE may progress to dysplasia.
Studies suggest the annual cancer incidence with BE ranges from 0.1 to 2.0 % [ 1 – 3 ].
Although the risk of developing EAC from BE has been estimated to be 30-fold
above the general population [ 4 ], the absolute risk of developing cancer is low.
Risk factors for BE include male sex, white race, age older than 50 years, family
history of BE, increased duration of refl ux symptoms, smoking, and obesity [ 5 ].
Endoscopic screening for BE is controversial because no randomized controlled
trials have demonstrated decreased mortality in EAC as a result of screening
[ 6 – 8 ].
Histologically, BE can be graded as non-dysplastic (NDBE), indeterminate-
grade dysplasia (IGD), low-grade dysplasia (LGD), high-grade dysplasia (HGD),
intramucosal carcinoma (IMC), or invasive EAC [ 9 ]. IGD is typically an interim
diagnosis typically found in the presence of infl ammation or technical issues related
to the specimen precluding a defi nitive diagnosis of dysplasia.
The management of patients with BE involves 3 major elements: (1) treatment of
gastroesophageal refl ux disease (GERD), (2) surveillance of dysplasia, and (3)
treatment of dysplasia. Chemoprevention of BE to prevent EAC has also been
studied.
W.D. Leung and I. Waxman
203
Treatment of GERD
For patients with BE, GERD therapy with medication effective to treat GERD
symptoms and to heal refl ux esophagitis is clearly indicated, as for patients without
BE. However, some experts recommend initial therapy with proton pump inhibitor
(PPI) rather than a “step-up” approach to GERD in patients without BE [ 5 ].
However, evidence to support the use of acid suppression in patients with BE solely
to reduce the risk of progression to dysplasia or cancer is indirect and has not been
proven in clinical trials. In BE patients without GERD symptoms or endoscopic
evidence refl ux esophagitis, the risks and benefi ts of long-term PPI therapy should
be discussed with patients taking into account their overall health status and medi-
cation use.
Different strategies have been studied to determine if aggressive refl ux treatment
prevents progression of BE to cancer. In vitro studies suggest acid exposure to
metaplastic esophageal epithelium may stimulate markers of cell proliferation, and
PPIs may decrease it (and by inference carcinogenesis) [ 10 , 11 ]. Clinical studies
(mainly observational) suggested profound acid suppression by double-dose PPI
[ 12 ] or fundoplication [ 13 ] may result only in a small regression of BE. However, a
systemic review of 25 surgical studies found antirefl ux surgery reduced incidence of
EAC only in uncontrolled but not controlled studies [ 14 ]. Thus, aggressive attempts
to eliminate esophageal acid exposure for the prevention of EAC have not been
found to be helpful. This includes PPI use greater than once daily, esophageal PH
monitoring to titrate PPI dosing, and antirefl ux surgery.
Endoscopic Dysplasia Surveillance
A survival benefi t of endoscopic surveillance for dysplasia in BE patients has not
been demonstrated in randomized prospective trials. Such trials may be too large
and costly to perform. Therefore, BE surveillance assumes BE reduces survival and
surveillance can reduce mortality. Data supporting BE surveillance suggest it can
detect curable dysplasia in BE and treatment [ 6 , 15 – 18 ]. However, this data is
mainly observational, and few studies document the natural history of dysplasia.
Despite large disparities seen in results of available studies, the risk of EAC in
patients with BE is approximately 0.25 % per year [
19 ]. In patients with HGD, the
risk is 4–8 % per year [ 20 ]. In patients with LGD, the risk is poorly defi ned but
likely between rates in BE and HGD [
21 ].
However, available data suggest that EAC is an uncommon cause of death in
patients with BE. In a 2010 meta-analysis of BE studies [ 22 ], the incidence of mor-
tality from EAC was 3.0 per 1,000 person-years and 37.1 person-years due to other
causes. This is likely because many BE patients are elderly and pass away from
common diseases such as coronary artery disease rather than EAC. This questions
the value of surveillance in patients with BE; however, the benefi t may be greater in
15 Barrett’s Esophagus: Treatment Options and Management
204
younger patients. Moreover, incurable malignancies have been reported in patients
despite adherence to endoscopic surveillance programs [ 15 ]. Another issue with BE
surveillance is that random biopsy sampling techniques used are imperfect for
detecting dysplasia, which is often patchy. Molecular markers such as p53, cyclin
D1 expression, and abnormal cellular DNA content by fl ow cytometry are promis-
ing markers associated with carcinogenesis, but none have been proven for routine
clinical use [ 5 ]. According to the 2011 American Gastroenterological Association
guidelines [ 5 ], patients with verifi ed BE, with no dysplasia after extensive biopsy
sampling, should undergo surveillance endoscopy every 3–5 years and patients with
LGD every 6–12 months. Surveillance in HGD will be discussed later.
Endoscopic Evaluation
Procedure Overview
BE endotherapy is performed most commonly on an outpatient basis. The proce-
dure can be performed with moderate sedation in some cases, although facilities are
increasingly utilizing monitored anesthesia care or general anesthesia as the pre-
ferred approach. For elective cases, patients should fast for 2 h (clear liquids) and
8 h (solid food) before the procedure. Ideally, anticoagulants (e.g., warfarin) and
antiplatelet agents (e.g., clopidogrel) should be held for 5–7 days, particularly in the
setting of endoscopic resection maneuvers. As a general rule, an international nor-
malized ratio <1.5 and platelet count >50,000 are preferred. Aspirin ≤325 mg by
mouth daily probably does not impact the risk of post-procedure hemorrhage.
For BE endotherapy, patients undergoing standard esophagogastroduodenos-
copy (a.k.a. upper endoscopy) are typically sedated in the left lateral position.
Following either procedure, patients who are at a moderate to high risk for compli-
cations should be kept fasting or advanced to clear liquids only and resume normal
diet the next morning in the absence of concerning signs/symptoms. Patients who
are at low risk of complications can gradually advance their diet over 4–6 h.
Endoscopic Assessment
BE is typically diagnosed endoscopically by a salmon or pink color (Fig. 15.1 ) on a
background of light gray squamous esophageal epithelium. However, histologic
exam of biopsies is required to confi rm the diagnosis.
Detection and diagnosis of BE by white light endoscopy alone has a sensitivity
from 80 to 90 % [ 23 , 24 ]. Nodules, ulcers, and other mucosal abnormalities should
have targeted biopsies because they are more likely to have dysplasia or cancer.
Adjunctive techniques to increase the sensitivity of BE detection include
W.D. Leung and I. Waxman