JOURNAL OF LAPAROENDOSCOPIC & ADVANCED SURGICAL TECHNIQUES

Volume 26, Number 0, 2016 Full Report

ª Mary Ann Liebert, Inc.
DOI: 10.1089/lap.2015.0530

A Modern Approach to the Surgical Treatment

of Gastroesophageal Reflux Disease

Talar Tatarian, MD, Michael J. Pucci, MD, FACS, and Francesco Palazzo, MD, FACS

Abstract

Gastroesophageal reflux disease (GERD) is a common disorder that can cause a variety of typical and atypical
symptoms. Although most patients can be rendered asymptomatic with medical treatment, some experience
persistent breakthrough symptoms. A long history of GERD is associated with the risk for the development of
Barrett’s esophagus and ultimately esophageal carcinoma. Although often underutilized, minimally invasive
antireflux surgery can help manage these patients. However, thorough evaluation and accurate diagnosis of
GERD and its underlying pathophysiology are critical in ensuring successful surgical treatment. This review
offers a stepwise approach to the diagnostic workup of GERD and how to appropriately tailor available surgical
treatments to specific patient subgroups.

Introduction In order to properly and successfully treat GERD, it is of

paramount importance to understand its underlying patho-

G astroesophageal reflux disease (GERD) is a highly

prevalent disorder that affects between 18% to 27% of
North Americans.1,2 Patients with GERD may experience
‘‘typical’’ symptoms (heartburn, regurgitation, dysphagia,
globus sensation) or ‘‘atypical’’ extraesophageal symptoms
(asthma, cough, hoarseness, aspiration, shortness of breath),
while additionally manifesting endoscopic signs of mucosal
inflammation or damage (erosive esophagitis) or no obvious
mucosal abnormality (nonerosive reflux disease).3–5 While
generally excellent relief of symptoms can be achieved via
medical therapy with proton pump inhibitors (PPIs), as many
as 30% to 40% of patients may experience persistent break-
through symptoms with significant impact on their quality of
life.6–9 Even more concerning is the increased risk of de-
veloping intestinal metaplasia with goblet cells (Barrett’s
esophagus [BE]) and esophageal adenocarcinoma in patients
with GERD. Although PPIs will decrease the acidity of the
refluxate, they do not affect the alkaline component of reflux,
nor do they decrease the number of episodes and proximal
extension of reflux.10 In a recent 5-year follow-up of subjects
enrolled in the ProGERD study, it was seen that under routine
clinical care, approximately 6% of patients with nonerosive
reflux disease progressed to BE.11 In those patients with mild
or severe esophagitis, the rates of development of BE were
12% and 20%, respectively. Once diagnosed with BE, pa-
tients are at increased risk of developing esophageal adeno-
carcinoma, at an estimated incidence of 0.5% per year.12
physiology, which goes beyond gastric acid production, cur-
rently the only target of medical therapy. Essentially, GERD is
caused by the breakdown of one or more components of the
antireflux barrier. This barrier is predominantly dependent on a
competent lower esophageal sphincter (LES), which can be
made defective by decreased intrinsic pressure, overall length,
or intraabdominal length, as seen with hiatal hernia.13 The
competence of the LES also relies on effective esophageal
peristalsis and gastric motility, as gastric distension decreases
LES length and increases the reflux of gastric contents into the
esophagus.13 Thus, defective function of any component of the
antireflux barrier can ultimately result in GERD.4,13,14 The role
of increased intraabdominal pressure (seen in obese patients)
as a cofactor in the pathophysiology of GERD is still largely
unknown. Most experts agree on the fact that the treatment of
severe reflux in morbidly obese patients should include a dif-
ferent strategic approach than the one used for patients with a
normal body mass index (BMI).
The complexity of GERD and the variability in its pre-
sentation make its diagnosis and subsequent treatment a
challenge. Deciding which patients have failed medical
management and what is the next intervention is a matter of
debate. However, it is clear is that all patients should undergo
a thorough workup in order to confirm the diagnosis and to
evaluate the integrity of the various components of the anti-
reflux barrier. In properly selected patients surgical therapy in
the hands of an experienced surgeon can achieve long-term

The Jefferson Gastroesophageal Center, Department of Surgery, Sidney Kimmel Medical College of Thomas Jefferson University
Hospital, Philadelphia, Pennsylvania.

1
2 TATARIAN ET AL.
satisfactory results.15 In this review we propose a stepwise
approach to the available surgical options for the treatment of
GERD to specific patient subgroups. There are currently
available endoscopic treatment options for the management
of GERD, most with no or limited long-term data on efficacy;
these will not be discussed in this review.
Patient Selection: Who Should Be Referred
for Surgical Evaluation?
The overwhelming majority of patients suffering from
GERD are managed medically. Although available medical
options will suffice for the majority of patients, a significant
group of patients will experience persistence of symptoms,
progression of disease, or development of complications de-
spite maximal medical therapy. These patients should be re-
ferred for surgical consultation.4 Despite the advances and
refinement of available surgical options, there has been a
steady decline in the number of antireflux surgeries performed
in the United States during the last 20 years, with only 18,780
cases in 2010 (Fig. 1).16–19 This decline is likely attributed to
several factors. One important hurdle is the general misun-
derstanding and fear from referring physicians about the long-
term morbidity and effectiveness of surgical treatment. The
development of endoscopic therapies and the availability of
over-the-counter PPIs, both perceived as less invasive inter-
ventions, have additionally influenced the fact that fewer pa-
tients are being seen for surgical consultation.7,16 However,
with as many as 30%–40% of GERD patients experiencing
poor symptom control with PPIs,6–9 there is a large subgroup
of patients who deserve closer attention and evaluation.
The Society of American Gastrointestinal and Endoscopic
Surgeons (SAGES) 2010 guidelines state that antireflux sur-
gery should be considered in the following clinical scenarios4:
1. Failure of medical management (i.e., persistent symp-
toms, severe regurgitation, side effects of medications).
2. Patient concerns regarding quality of life, expense of
medications, and need for lifelong therapy despite suc-
cessful medical management.
3. Presence of complications of GERD (BE, peptic stricture).
4. Presence of extraesophageal manifestations of GERD
(asthma, aspiration, cough, chest pain, hoarseness).
FIG. 1. Annual rate of antireflux surgeries performed in
the United States from 1990 to 2010.
The Antireflux Barrier
The antireflux barrier is composed of multiple physiologic
and anatomic components that work together to prevent the
reflux of contents from high-pressure distal compartments to
low-pressure proximal compartments.13 The most obvious
element of the antireflux barrier is the LES, which serves as a
barrier between the high-pressure stomach and low-pressure
esophagus. This physiologic sphincter can be rendered in-
competent by changes in its intrinsic pressure, overall length,
and position.20,21 Patients with an intrinsic pressure of 6 mm
Hg or less, a resting LES length of 2 cm or less, or an in-
traabdominal length of 1 cm or less are at increased risk of
reflux. Other factors shown to decrease LES competence
include laxity of the diaphragmatic crura and phrenoeso-
phageal membrane, flattening of the angle of His, and de-
velopment of a hiatal hernia.14 The integrity of the antireflux
barrier at the gastroesophageal junction is maintained by the
LES and crura. Crural laxity and disruption of the phrenoe-
sophageal ligament can contribute to hiatal hernia formation
and subsequent LES dysfunction due to shortened in-
traabdominal length and exposure to negative intrathoracic
pressure. Even in the absence of hiatal hernia, intrinsic loss of
LES tone, increased frequency of LES transient relaxation,
and reduction of LES length (both overall and intraabdominal
length) can result in significant reflux.
Equally important to the antireflux barrier is the function
of the esophagus and stomach.13 Effective esophageal peri-
stalsis is required for appropriate LES relaxation and esopha-
geal clearance. Additionally, ineffective gastric emptying may
lead to gastric distension resulting in shortening of the LES,
thus decreasing LES competence. Appreciation of the com-
plexity of the antireflux barrier and understanding its various
components are essential in evaluating and treating patients
with GERD.
Presurgical Evaluation of Reflux
In evaluating a patient for invasive therapy, it is important
to first confirm the presence of GERD and then to study its
underlying pathophysiology in order to recommend the ap-
propriate treatment that affords the patient the highest chance
for success. A careful history with review of presenting
symptoms is an important first step. Then direct investigation
of the antireflux barrier is necessary. Past experience has
found that successful outcomes are most likely in those with
typical symptoms of GERD, increased esophageal acid ex-
posure confirmed on pH testing, and some level of symp-
tomatic response to PPI therapy.22
Both SAGES and the European Association of Endoscopic
Surgery (EAES) recommend esophagogastroduodenoscopy to
confirm the diagnosis of GERD and to obtain tissue biopsies.4,5
The diagnosis is firmly established with the presence of se-
vere reflux esophagitis or long-segment BE (q3 cm Barrett’s
metaplasia).7 If there is diagnostic uncertainty or in patients with
only mild or no erosive esophagitis or short-segment BE, pH
monitoring with or without impedance testing should be used.7
Once the diagnosis of GERD is confirmed, esophageal
manometry should be performed to evaluate esophageal
motility. Although manometry is not necessary for the di-
agnosis for GERD, it is considered mandatory for presurgical
evaluation to help identify conditions in which an antireflux
procedure may be inappropriate or contraindicated, such as
SURGICAL TREATMENT OF GERD
achalasia, ineffective esophageal motility, severe hypomoti-
lity secondary to scleroderma, nutcracker esophagus, or distal
esophageal spasm.6,7
A barium swallow is useful to delineate the anatomy of the
esophagus and to identify a hiatal hernia, diverticulum, peptic
stricture, or shortened esophagus.4,21 It can also evaluate the
function of the esophageal body and LES.21 Gastric emptying
studies should be considered in select populations such as
diabetics and those in whom typical symptoms are associated
with nausea and vomiting.5 This can help identify delayed
gastric emptying, gastric outlet obstruction, or gastroparesis
as the underlying cause of reflux.
Strategic Approach to Surgical Decision-Making
When deciding on an appropriate therapeutic approach, it
is important to closely evaluate all diagnostic studies to de-
termine the underlying pathophysiology causing reflux.
Thus, factors that are critical in surgical decision-making
are as follows:
1. Presence/absence of GERD by esophagogastroduodeno-
scopy/pH study.
FIG. 2. Proposed algorithm for the evaluation and treatment of patients with gastroesophageal reflux disease (GERD).
BMI, body mass index (in kg/m2); DES, diffuse esophageal spasm; EGD, esophagogastroduodenoscopy; HH, hiatal hernia;
LRYGB, laparoscopic Roux-en-Y gastric bypass.
3
2. Assessment of esophageal motility by esophageal
manometry.
3. Presence/absence of hiatal hernia.
4. Obesity (BMI >35–40 kg/m2).
5. Assessment of gastric motility.
In the following paragraphs we describe our rationale for
surgical treatment of GERD patients. These general guiding
principles are further outlined in Figure 2.
Severe GERD with minimal or no anatomic disruption
(LES dysfunction)
In the setting of normal esophageal motility with a weak-
ened LES, patients with poorly controlled GERD have two
surgical options: laparoscopic fundoplication (total or partial)
or magnetic sphincter augmentation of the LES.
The current gold standard in this setting is represented by
laparoscopic total or partial fundoplication. Long-term data
have shown that over 90% of patients have continued
symptom control with 70%–92% of patients remaining off
daily antireflux medication.23 Postoperative side effects
include transient dysphagia, bloating, early satiety, and
4 TATARIAN ET AL.
flatulence.4,5,23,24 If a hiatal hernia is present, particularly one
larger than 3 cm, fundoplication is required to restore the
length and competence of the LES. A total fundoplication is
preferred in the setting of normal esophageal motility and, as
stated above, is a well-proven, safe, and durable intervention
in experienced hands.4,21
Critical to the success of this procedure is the need to
follow key technical steps. These include the following:
 Complete crural dissection with identification and
preservation of both anterior and posterior vagus
nerve and reduction/excision of hiatal hernia sac if
present.
 Circumferential dissection of the esophagus and posterior
mediastinum to obtain adequate abdominal esophageal
length (3 cm).
 Crural closure.
 Mobilization of gastric fundus with division of short
gastric vessels.
 Fundoplication.
The last two steps have been a source of long debate
in the surgical community, and although some authors,
based on data from randomized controlled trials,25 may
recommend against routine division of the short gastric
vessels, all agree that a form of fundoplication—partial or
complete—is a mandatory final step for a successful anti-
reflux procedure.
If preoperative evaluation indicates evidence of esoph-
ageal dysmotility, continued medical treatment or at a
maximum laparoscopic partial fundoplication should be
considered depending on the severity and type of dysmo-
tility. Ineffective esophageal motility (ineffective esoph-
ageal manometry-contraction amplitudes of <30 mm Hg
and <50% peristaltic waves) warrants partial fundoplica-
tion,5,21,26 whereas achalasia (aperistalsis) and diffuse
esophageal spasm (high-amplitude nonperistaltic contrac-
tions) are considered contraindications for antireflux sur-
gery.7 Studies have shown that partial fundoplication is as
effective as total fundoplication in controlling GERD with
less postoperative dysphagia up to 5 years after surgery.27
In addition, SAGES and EAES guidelines both advocate
crural approximation and hiatal repair at the time of anti-
reflux surgery.4,5
A recent addition to the surgeon’s armamentarium is mag-
netic sphincter augmentation. This intervention has been
studied in patients with severe GERD—proven by pH study—
and with normal esophageal motility without hiatal hernia or
with a hiatal hernia of less than 3 cm, as well as a BMI below
35 kg/m2.7,28 This is a novel Food and Drug Administration–
approved therapy that strengthens the antireflux barrier by
placing an expandable ring of titanium beads around the LES,
which externally augments its resting pressure. The anatomy
of the stomach is left unaltered, minimizing the risk of side
effects associated with other antireflux operations, such as
dysphagia and inability to belch or vomit.29 Clinical trials to
date have demonstrated normalization or 50% reduction of
esophageal acid exposure in 64%–80% of patients.28–32 Post-
operative dysphagia was reported in 43%–68% of patients but
was self-limited in the majority of patients, resolving by Week
8–9 in most patients. We believe this is a very promising in-
tervention and should be considered as first-line treatment for
patients with severe GERD with minimal or no anatomic
disruption and normal esophageal motility; results from long-
term studies are still needed to confirm 10-year safety and
continued efficacy.
Severe GERD with significant anatomic disruption
(hiatal hernia >3 cm)
In this setting the patient should be recommended to un-
dergo a laparoscopic total or partial fundoplication following
the strict surgical criteria described in the above paragraph.
Morbid obesity (BMI >35 kg/m2)
Obesity is an independent risk factor for the development
of GERD and progression to BE, ultimately placing this
population at increased risk for esophageal adenocarcino-
ma.6,33 There are several proposed mechanisms linking
obesity to GERD, including increased gastric distension
leading to increased frequency of transient LES relaxations33
and displaced LES secondary to increased intraabdominal
pressure.34 Traditional antireflux operations do not correct
the underlying problem, and higher failure rates have been
reported in obese individuals compared with normal-weight
counterparts.35,36 The most recent SAGES and EAES guide-
lines recommend gastric bypass in the morbidly obese patient
(BMI >35 kg/m2) with uncontrolled GERD as it simulta-
neously treats GERD, provides weight loss, and improves
the associated comorbidities of both conditions.4,5
Abnormal Gastric Emptying: Gastroparesis
An important consideration in patients refractory to
medical therapy of GERD is whether or not an underlying
gastric emptying component may be present. This is partic-
ularly relevant in diabetics, in whom gastroparesis is a
common complication. Often the symptoms of GERD and
gastroparesis overlap, making the diagnosis and treatment a
challenge. When evaluating a patient for antireflux surgery,
the surgeon should obtain a thorough history and physical,
and, if warranted, a gastric emptying study should be per-
formed to confirm the diagnosis of gastroparesis. In the set-
ting of gastroparesis, delayed gastric emptying causes gastric
overdistension, followed by subsequent shortening of the
LES and reflux of gastric content into the esophagus. In these
patients, fundoplication alone can worsen symptoms of early
satiety, nausea, and bloating. Although the treatment of
gastroparesis is predominantly medical, surgery should be
considered in severe refractory cases. Options include py-
loromyotomy, pyloroplasty, subtotal gastrectomy, gastric
bypass, and gastric electrical stimulation, to name a few. The
diagnostic workup and choice of operation are beyond the
scope of this article. However, the presence of gastroparesis
in the patient with GERD should be considered during pre-
operative evaluation for antireflux surgery in the above-
mentioned clinical settings.
Conclusions
Although the majority of uncomplicated GERD patients can
be appropriately treated with medical therapy, there remains a
group of patients who require a more tailored approach for
symptom relief and prevention of disease progression. Treat-
ment of the GERD patient who is a ‘‘nonresponder’’ to medical
SURGICAL TREATMENT OF GERD
treatment requires a thorough understanding of the antireflux
barrier and evaluation of its components. This evaluation of the
reflux barrier allows surgeons to appropriately tailor the surgical
approach with hopes of excellent long-term outcomes, along
with prevention of the sequelae associated with severe GERD.
Disclosure Statement
No competing financial interests exist.
References
1. El-Serag HB, Sweet S, Winchester CC, Dent J. Update on
the epidemiology of gastro-oesophageal reflux disease: A
systematic review. Gut 2014;63:871–880.
2. Dent J, El-Serag HB, Wallander MA, Johansson S. Epi-
demiology of gastro-oesophageal reflux disease: A sys-
tematic review. Gut 2005;54:710–717.
3. Vakil N, van Zanten SV, Kahrilas P, Dent J, Jones R; Global
Consensus Group. The Montreal definition and classification
of gastroesophageal reflux disease: A global evidence-based
consensus. Am J Gastroenterol 2006;101:1900–1920; quiz
1943.
4. Stefanidis D, Hope WW, Kohn GP, Reardon PR, Richardson
WS, Fanelli RD, et al. Guidelines for surgical treatment of
gastroesophageal reflux disease. Surg Endosc 2010;24:
2647–2669.
5. Fuchs KH, Babic B, Breithaupt W, Dallemagne B, Fingerhut
A, Furnee E, et al. EAES recommendations for the man-
agement of gastroesophageal reflux disease. Surg Endosc
2014;28:1753–1773.
6. Katz PO, Gerson LB, Vela MF. Guidelines for the diag-
nosis and management of gastroesophageal reflux disease.
Am J Gastroenterol 2013;108:308–328; quiz 329.
7. Perry KA, Pham TH, Spechler SJ, Hunter JG, Melvin WS,
Velanovich V. 2014 SSAT State-of-the-Art Conference:
Advances in diagnosis and management of gastroesopha-
geal reflux disease. J Gastrointest Surg 2015;19:458–466.
8. Fass R, Sifrim D. Management of heartburn not responding
to proton pump inhibitors. Gut 2009;58:295–309.
9. El-Serag H, Becher A, Jones R. Systematic review: Per-
sistent reflux symptoms on proton pump inhibitor therapy
in primary care and community studies. Aliment Pharmacol
Ther 2010;32:720–737.
10. Hemmink GJ, Bredenoord AJ, Weusten BL, Monkelbaan JF,
Timmer R, Smout AJ. Esophageal pH-impedance monitor-
ing in patients with therapy-resistant reflux symptoms: ‘On’
or ‘off’ proton pump inhibitor? Am J Gastroenterol 2008;
103:2446–2453.
11. Malfertheiner P, Nocon M, Vieth M, Stolte M, Jaspersen D,
Koelz HR, et al. Evolution of gastro-oesophageal reflux dis-
ease over 5 years under routine medical care—The ProGERD
study. Aliment Pharmacol Ther 2012;35:154–164.
12. Yousef F, Cardwell C, Cantwell MM, Galway K, Johnston
BT, Murray L. The incidence of esophageal cancer and high-
grade dysplasia in Barrett’s esophagus: A systematic review
and meta-analysis. Am J Epidemiol 2008;168:237–249.
13. Peters JH, DeMeester TR. The gastroesophageal barrier. In:
Yeo CJ (ed). Shackelford’s Surgery of the Alimentary
Tract. Philadelphia: Elsevier Saunders, 2013, pp. 194–200.
14. Wykypiel H, Gadenstätter M, Granderath FA, Klingler PJ,
Wetscher GJ. Pathophysiology of gastro-oesophageal reflux
disease (GERD) with respect to reflux-induced carcino-
genesis. Eur Surg 2002;34:296–302.
5
15. Watson DI, Baigrie RJ, Jamieson GG. A learning curve for
laparoscopic fundoplication. Definable, avoidable, or a
waste of time? Ann Surg 1996;224:198–203.
16. Finks JF, Wei Y, Birkmeyer JD. The rise and fall of anti-
reflux surgery in the United States. Surg Endosc 2006;20:
1698–1701.
17. Funk LM, Kanji A, Scott Melvin W, Perry KA. Elective
antireflux surgery in the US: An analysis of national trends
in utilization and inpatient outcomes from 2005 to 2010.
Surg Endosc 2014;28:1712–1719.
18. Finlayson SR, Laycock WS, Birkmeyer JD. National trends
in utilization and outcomes of antireflux surgery. Surg
Endosc 2003;17:864–867.
19. Wang YR, Dempsey DT, Richter JE. Trends and periopera-
tive outcomes of inpatient antireflux surgery in the United
States, 1993–2006. Dis Esophagus 2011;24:215–223.
20. Bonavina L, Evander A, DeMeester TR, Walther B, Cheng
SC, Palazzo L, et al. Length of the distal esophageal sphinc-
ter and competency of the cardia. Am J Surg 1986;151:
25–34.
21. Worrell SG, Greene CL, DeMeester TR. The state of sur-
gical treatment of gastroesophageal reflux disease after five
decades. J Am Coll Surg 2014;219:819–830.
22. Campos GM, Peters JH, DeMeester TR, Oberg S, Crookes
PF, Tan S, et al. Multivariate analysis of factors predicting
outcome after laparoscopic Nissen fundoplication. J Gas-
trointest Surg 1999;3:292–300.
23. Morgenthal CB, Shane MD, Stival A, Gletsu N, Milam G,
Swafford V, et al. The durability of laparoscopic Nissen
fundoplication: 11-year outcomes. J Gastrointest Surg 2007;
11:693–700.
24. Galmiche JP, Hatlebakk J, Attwood S, Ell C, Fiocca R,
Eklund S, et al. Laparoscopic antireflux surgery vs
esomeprazole treatment for chronic GERD: The LOTUS
randomized clinical trial. JAMA 2011;305:1969–1977.
25. Engstrom C, Jamieson GG, Devitt PG, Watson DI. Meta-
analysis of two randomized controlled trials to identify
long-term symptoms after division of the short gastric
vessels during Nissen fundoplication. Br J Surg 2011;98:
1063–1067.
26. Swanström LL, Dunst CM. Partial fundoplications. In: Yeo
CJ (ed). Shackelford’s Surgery of the Alimentary Tract.
Philadelphia: Elsevier Saunders, 2013, pp. 237–245.
27. Varin O, Velstra B, De Sutter S, Ceelen W. Total vs par-
tial fundoplication in the treatment of gastroesophageal
reflux disease: A meta-analysis. Arch Surg 2009;144:
273–278.
28. Bonavina L, Saino G, Lipham JC, Demeester TR. LINX
Reflux Management System in chronic gastroesophageal
reflux: A novel effective technology for restoring the nat-
ural barrier to reflux. Therap Adv Gastroenterol 2013;6:
261–268.
29. Ganz RA, Peters JH, Horgan S. Esophageal sphincter de-
vice for gastroesophageal reflux disease. N Engl J Med
2013;368:2039–2040.
30. Bonavina L, Saino GI, Bona D, Lipham J, Ganz RA, Dunn
D, et al. Magnetic augmentation of the lower esophageal
sphincter: Results of a feasibility clinical trial. J Gastro-
intest Surg 2008;12:2133–2140.
31. Bonavina L, DeMeester T, Fockens P, Dunn D, Saino G,
Bona D, et al. 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.
6 TATARIAN ET AL.
32. Lipham JC, DeMeester TR, Ganz RA, Bonavina L, Saino
G, Dunn DH, et al. The LINX reflux management system:
Confirmed safety and efficacy now at 4 years. Surg Endosc
2012;26:2944–2949.
33. El-Serag HB, Graham DY, Satia JA, Rabeneck L. Obesity
is an independent risk factor for GERD symptoms and
erosive esophagitis. Am J Gastroenterol 2005;100:1243–
1250.
34. Braghetto I, Korn O, Csendes A, Gutierrez L, Valladares H,
Chacon M. Laparoscopic treatment of obese patients with
gastroesophageal reflux disease and Barrett’s esophagus: A
prospective study. Obes Surg 2012;22:764–772.
35. Perez AR, Moncure AC, Rattner DW. Obesity adversely
affects the outcome of antireflux operations. Surg Endosc
2001;15:986–989.
36. Morgenthal CB, Lin E, Shane MD, Hunter JG, Smith CD.
Who will fail laparoscopic Nissen fundoplication? Pre-
operative prediction of long-term outcomes. Surg Endosc
2007;21:1978–1984.
Address correspondence to:
Francesco Palazzo, MD, FACS
The Jefferson Gastroesophageal Center
Department of Surgery
Thomas Jefferson University Hospital
1100 Walnut Street, Suite 500
Philadelphia, PA 19107
E-mail: Francesco.Palazzo@jefferson.edu