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76 C. Barbon et al.
Bilitec consists of a fiber optic system for
duodeno-gastroesophageal monitoring. It allows
detecting duodenal reflux concomitantly in different sites of the upper GI, and it can be coupled
with pH monitoring. It has been noticed that
patients with concomitant gastric and duodenal
reflux have a worse mucosal injury and higher
severity of complications, compared to patients
who present only one of the two components.
Furthermore, patients with BE have a higher exposure to duodenal juice [23,24,25] than those
who do not have metaplasia.
Treatment
There are three main treatment options for reflux-induced esophagitis: medical therapy, endoscopic treatment, and surgery. However, a multidisciplinary approach is often useful to address
erosive esophagitis.
The therapeutic role and effectiveness of lifestyle modifications are controversial; however,
these are often among the first advices given to
patients after the diagnosis of GERD. The general recommendations are to avoid foods that
stimulate LES relaxation such as tea, coffee,
peppermint, chocolate, alcoholic beverages, and
irritant foods such as citrus fruits and tomatoes.
Moreover, it can be useful eating several hours
before lying down, sleeping with the head lifted
by 20 cm to favor esophageal clearance, and quitting smoking. Weight loss in overweight patients
has been shown to improve symptoms even in
refractory cases [26], likely by decreasing intraabdominal pressure.
Medical therapy is the first line of treatment
[27], with PPIs being the most effective group
of medications [28]. PPIs should be prescribed
to all patients with moderate to severe symptoms, or with a confirmed diagnosis of erosive
esophagitis. PPIs are the most common class of
medications prescribed in the USA [29]; they
are very effective in healing esophagitis and
improving its symptoms, and they are the most
useful drugs in maintaining erosive esophagitis
in remission. They should be initially prescribed
at their minimum effective dose [30], and dose
adjustment should be considered after evaluation of patient’s response. After 1–2 months of
therapy, erosive esophagitis is healed in 84–95 %
of patients; however, symptoms resolve only in
75–85 % [4]. PPIs block the hydrogen–potassium
ATPase (H+/K+ATPase) by covalently binding
it on to the apical surface of the parietal gastric
cells. PPIs do not decrease the amount of reflux,
but they only make the gastric content less harmful by modifying the acidic and nonacidic content: acid decreases from 45 to 3 %, while the
nonacidic fraction increases form 55–97 % [31].
As a consequence, the reflux still occurs, but it
is not acidic, with a pH commonly raised above
4. Although duodenal reflux is not affected by
PPIs, and some authors suggested that their use
might increase its damaging potential [32]: bile
acids are inactivated when surrounded by acidic
environment, but after PPI therapy, the pH raises
above 4 and bile salts are converted to their ionized form, which are able to cross epithelial cell
membrane and cause intracellular damage.
PPIs have also reduced efficiency in treating extra-esophageal symptoms [33], which are
commonly caused by the presence of reflux more
than its quality.
Patients with esophagitis often require a lifelong therapy since medications do not address
the disease’s etiology; in fact, about 80 % of
patients will have recurrence of esophagitis approximately 1 year after the discontinuation of
therapy [33].
Side effects of PPIs occur in about 1–5 % of
patients and consist mostly of diarrhea, headache,
constipation, abdominal pain, nausea, and rash
[29]; when severely affecting the patients, they
are managed by switching to a different medication, since a considerable degree of subjective
variability exists, even though most of the side effects are class dependent. PPIs are generally safe,
but concerns have been raised during prolonged
use. The continuous suppression of gastric acid
causes hypo- or achlorhydria, which might affect
some nutrients’ absorption such as iron, vitamin
B12, magnesium, calcium, and proteins [4]. Hypochlorhydria also decreases the acidic natural
defense against bacteria, increasing the odds of
overgrowth; an increased risk for Clostridium
777 Severe Reflux-Induced Esophagitis
difficile, Salmonella, and Campylobacter-related
diarrhea has been reported [34]. Increased incidence of community-acquired pneumonia (CAP)
has also been associated with PPI use [35].
Histamine2-receptor antagonists (H2RA)
were also prescribed in the past, but several trials have established the superiority of PPIs over
H2RA both in symptoms control and in esophageal healing, due to their capability of blocking
the final step of acid secretion.
Surgery. Elective ARS can offer a definitive
cure for esophagitis in selected patients, since it
reestablishes a competent LES and allows for
repair of concurrent hiatal hernias. Surgery has
been shown to have the best outcome in patients
with typical symptoms, objectively proven reflux, and good response to medical therapy [36].
The most common indications for ARS are dependence upon medical therapy, intolerance or
noncompliance to therapy, and life-lasting treatment for young patients. ARS eliminates both
acidic and biliary reflux in >
BE [37
], and the effect on alkaline reflux repre-
90 % of patients with
sents a major advantage of ARS over medical
therapy. Randomized data have shown no difference in remission rate between maintenance PPI
treatment and laparoscopic Nissen fundoplication at 5-year follow-up. The same study showed
that while acid regurgitation was more prevalent
in the PPI group, side effects of fundoplication,
such as dysphagia, bloating, and flatulence, were
more represented in the surgical group [38].
ARS has been reported to be more successful
than medical therapy in stopping the progression
to BE and adenocarcinoma [39]. Moreover, some
studies have shown a higher likelihood of regression of Barrett’s metaplasia and dysplasia after
ARS [40,41].
The most used surgical procedure is the Nissen fundoplication, introduced in 1956, which
consists of confectioning a 360° gastric wrap
around the esophagus. Floppy Nissen is a modification of the original technique, which allows
reducing dysphagia and gas bloat syndrome that
occurred in as many as 40
% of the patients with
the traditional Nissen procedure. Floppy Nissen
involves creation of a 2–3-cm-long gastric wrap
around a bougie dilator (52–56 Fr).
In patients with severe motility
disorders or
suboptimal esophageal peristalsis, a partial fundoplication is generally performed in order to
lower the risk of postoperative dysphagia. Partial
posterior fundoplication (270° Toupet) has been
introduced in the 1960s as an alternative to the
Nissen fundoplication. In the short term, Toupet
had good results in terms of reflux control, and it
has been shown to decrease postsurgical dysphagia and bloating with respect to Nissen [4]. However, some studies report that it is less effective
than total fundoplication, with a recurrence rate
of reflux as high as 50
% after 5 years [42,43
].
ARS is mostly performed laparoscopically,
since minimally invasive techniques grant significant advantages over open ARS, in terms of
decreased pain, faster recovery, shorter length of
hospital stay, and low morbidity and mortality.
Surgical complications occur in less than 5
of patients and mostly
consist of bleeding and
%
damage to the surrounding structures (spleen,
esophagus, stomach, and vagus nerve). Postsurgical course is typically characterized by feeling
of fullness and mild swallowing difficulties, especially with solid foods, but most patients return
to normal after 6 weeks [44].
Nissen fundoplication has been reported to resolve reflux symptoms in up to 95
% of patients.
Its most common long-term complication is dysphagia,
3 to 25
occurring with a frequency ranging from
%, depending on the published series, and
eventually leading to reoperation in up to 15 %
of patients. Less frequently patients
complain of
early satiety, bloating, and flatulence.
ARS has been reported to heal esophagitis in
up to 87
provement in 95
after fundoplica
and
% of patients [45
], with symptoms im-
%. Recurrence of esophagitis
tion ranges from 5 to 15
can lead to reoperation in about 6
% [46]
% of pa
tients [47]. Recurrence of esophagitis is usually
associated with a failed surgical procedure.
Surgical costs are justified by long-term success, savings on prolonged medical therapy, overall better control of disease, and increased healthrelated quality of life (HRQoL) when compared
to PPIs [48,49]. Importantly, according to some
authors, ARS is superior to medical therapy in
limiting the progression of low-grade dysplasia
78 C. Barbon et al.
Fig. 7.1 Laparoscopic view of floppy Nissen fundoplica-
tion
(LGD) to high-grade dysplasia (HGD) or cancer
[50], and it leads to regression from LGD to BE
in 93.8 % versus only 63.2 % with medical therapy [50]. This statistically relevant difference is
probably due to the ability of surgery of limiting
not only the acidic reflux, but also the biliopancreatic one.
New minimally invasive approaches for ARS
include placement of a magnetic device around
the GEJ to help maintaining LES continence
or implantation of an electrical stimulator connected to electrodes in the LES that stimulates
contractions. The LINX Reflux system used for
sphincter augmentation through the employment
of titanium beads showed encouraging results
for uncomplicated GERD, reducing acid exposure with fewer side effects than ARS [51]. Even
though these novel techniques have good potential, further studies are required to confirm their
efficacy.
Finally, it should not be forgotten that although
ARS lowers the risk of progression to cancer, it
does not eliminate the risk of neoplastic progression in patients with BE, especially if there is
recurrence of GERD. Endoscopic surveillance
after surgery is recommended for patients with
BE (Fig. 7.1).
Endoscopic techniques are relatively new
approaches appealing for high-risk patients.
These techniques include transoral incisionless
fundoplication, suturing devices that create a
gastroesophageal valve from inside the stomach,
transmural fasteners, staplers, and radiofrequency devices used to induce muscular hypertrophy
at the level of LES and gastric cardia. The ef-
Fig. 7.2 Endoscopic view of grade C esophagitis with
ulcerations
ficacy of the latter approach may be due to increased wall thickness, LES pressure, decreased
TLESR, decreased tissue compliance, acid sensitivity, and exposure [52]. However, according to
some authors, endoscopic techniques are inferior
to surgery in terms of decreased esophageal acid
exposure, healing of esophagitis, and symptoms
resolution [4].
Complications
Complications of esophagitis are strongly related
to its chronicity, since continuous exposure to
gastroduodenal reflux can progressively aggravate the disease.
Ulcers (Fig. 7.2): Erosive esophagitis can
lead to ulcerations; these may be responsible for
significant morbidities such as severe upper GI
hemorrhages, strictures (12.5 %), and esophageal
perforations (3.4 %) [53]. Chronic blood loss
from active esophageal ulcers may cause iron deficiency anemia. Ulcerations are diagnosed with
endoscopy, and a biopsy is always indicated to
rule out malignancy. Ulcers in reflux esophagitis
tend to be recurrent; therefore, appropriate therapy must be targeted to neutralize the underlying
acid reflux and allow tissue healing.
Esophageal shortening and narrowing
occur as a result of repeated, prolonged injury:
Acidic reflux causes inflammation, edema, and
797 Severe Reflux-Induced Esophagitis
Fig. 7.3 Barium esophagram showing esophageal stric-
ture
in the longrun destruction of muscolaris mucosae, leading to the formation of strictures at the
level of the circular muscle; eventually, when
fibrosis of the outer longitudinal muscle occurs
because of transmural inflammation, the esophagus shortens. Esophageal shortening may also
be found in patients with a failed antireflux procedure or with a mixed hiatal hernia that causes
the upward migration of the GEJ [54]. 2 –4 % of
patients undergoing antireflux procedures have a
short esophagus [55].
Short esophagus is addressed surgically, most
commonly using a Collis gastroplasty as an
esophageal lengthening procedure. This can be
completed laparoscopically, and an antireflux
procedure is routinely added.
Strictures (Fig. 7.3) are the result of chronic
inflammation and of repeated cycles of ulceration
and healing, with subsequent fibrous tissue and
collagen deposition, scar formation, and retraction. The process starts with a reversible phase
characterized by edema and muscular spasm and
then evolves to the formation of erosions. Location in distal esophagus, at the squamocolumnar
junction, is a hallmark of peptic strictures, which
are also usually shorter than 1 cm. Strictures
observed more proximally are unlikely due to
reflux. Peptic strictures can be found in 7–23 %
of patients with untreated GERD with severe
erosive esophagitis, mostly in the elderly, and
in 25–44
% of patients who concomitantly
have
BE [56]. Their incidence has decreased steeply
in parallel to the diffusion of PPIs. Factors predisposing to the development of peptic strictures
include prolonged reflux, hypotensive LES,
dysfunctional motility, hiatal hernia, bile reflux,
and advanced age [53]. Symptoms are relatively
nonspecific and influenced by stricture severity:
dysphagia is the most frequent and can be accompanied by typical GERD symptoms. Food stasis
causes halitosis and is also responsible for further
mucosal damage and aspiration pneumonia.
Strictures can be divided into simple and com-
plicated (Table 7.2) [57].
Alternatively, strictures can be classified into
three subtypes (mild, moderate, and severe),
according to the parameters such as diameter,
length, and difficulty in dilating the stricture
[58]; this distinction aims to help choosing the
most appropriate treatment for every subgroup.
Diagnostic workup for peptic strictures must
include endoscopy to perform biopsies and rule
out malignancies. Esophagram (Fig. 7.3) is very
helpful in visualizing the esophageal narrowing
and proves particularly valuable in severe strictures, when the endoscope cannot pass through.
Therapy’s aim is to improve dysphagia, and
avoid obstruction and recurrence.
Medical therapy plays a poor role once the
stricture is already established; however, PPIs
are fundamental to heal the concomitant esophagitis and prevent disease progression. Dilation is
the primary therapy [59] and should be the first
operative step: It can be attempted with the endoscope itself when the strictures are mild, but it is
usually performed through bougies (Savary-Gilliard or Maloney) or balloon-type dilators, with
or without guidewire assistance. Complex strictures often require guidewire and fluoroscopy for
safe placement of the dilators. Self-dilation can
seldom be offered to carefully selected patients
[37].
Dilation is generally safe; however, the potential risk of hemorrhage and perforation ranges between 0.1 and 0.4 % [59]. The occurrence
of procedural complications can be reduced by
performing the dilation progressively through
80 C. Barbon et al.
Table 7.2 Types of esophageal strictures [57]
Simple Symmetrical, focal, concentric, with an esophageal luminal diameter of > 12 mm allowing the
Complicated Long (>
endoscope passage
2 cm) irregular, narrowing the luminal diameter to less than 12 mm
multiple sessions and avoiding dilating more than
3 mm each time [37]. Dilation should be associated with either acid suppression medical therapy
or ARS to enhance success [60]. However, even
with aggressive therapy, only 60–70 % of patients
have complete resolution of symptoms, and multiple repeated dilations are often required [59]. To
date, no randomized controlled trials have compared ARS versus medical management and serial bougienage; however, a retrospective study
suggested that optimal reflux control with ARS
results in decreased need for repeated dilation
and better symptomatic outcome [61].
If satisfying dilation is not achieved after multiple sessions, strictures are deemed refractory,
and the use of endoprosthesis (metal or plastic
stent) should be considered [4]. Esophageal stenting and local steroid injections can be an auxiliary therapeutic option for refractory or recurrent
strictures; the latter in particular has the capacity
of inhibiting the inflammatory response, limiting
collagen deposition [62]. Combining these two
treatments with acid suppression therapy successfully reduces both the need for dilations and
the time between sessions [37]. Presence of hiatal
hernia, ineffective acidic therapy (low dose, poor
compliance), or alkaline reflux may predispose to
disease recurrence.
Rarely, esophagectomy is indicated for recurrent or refractory strictures with underlying
intractable esophagitis and a severely damaged
esophagus [58]. Most commonly, an esophagectomy is necessary with gastroplasty or colonic/
jejunum interposition [63].
Schatzki’s Rings are circular narrowed areas
constituted by esophageal and gastric mucosa
with fibrous and connective tissues, which are
usually observed at the GEJ. They have a similar
etiology to peptic strictures, and they also lead to
dysphagia causing food impaction in the esophageal lumen. If this event occurs abruptly, endoscopic food extraction is indicated; the procedure
is safer when performed with an endoscope cov-
Fig. 7.4 Endoscopic view of Barrett’s esophagus
ered by an overtube, in order to avoid aspiration
in the bronchial tree. Conversely, pushing food in
the stomach is not advisable as it may lead to perforation. Schatzki’s rings are diagnosed through
barium swallow and endoscopy. The therapy of
choice is bougie dilation associated with PPIs
that are administered after dilation, which dramatically reduce esophageal rings’ incidence and
recurrence.
Respiratory complications may arise in patients with esophagitis, mainly as a consequence
of long-standing GERD. Aspiration of acid and
alkaline reflux can acutely cause chemical pneumonia; chronic acid exposure may lead to asthma
and permanent lung damage such as fibrosis and
bronchiectasis. Both medical therapy and surgery are less successful in patients with respiratory symptoms than typical symptoms. However,
surgery offers the advantage of eliminating nonacid reflux episodes as well and therefore may be
more appropriate in these types of patients.
Barrett’s esophagus (Fig.
of the patients
with erosive esophagitis [6] show
7.4).
About 10
%
an intestinal type of metaplasia called BE, in
which patches of columnar epithelium with
typical intestinal goblet cells replace the normal stratified squamous esophageal epithelium
in the distal esophagus. Affected patients have
817 Severe Reflux-Induced Esophagitis
a higher acid exposure than those with erosive
and nonerosive esophagitis without BE [64]. The
metaplastic transformation occurs as an adaptive
response to injury exerted by reflux on the physiologic esophageal lining. High-grade esophagitis
has a high damaging potential, and its healing
through metaplastic columnar epithelium makes
the esophagus more resistant to reflux injury, but
at the same time, may trigger significant dysplastic changes: LGD, pre-invasive HGD, and adenocarcinoma. BE is a pre-cancerous condition
and needs to be identified and surveilled to allow
for prompt intervention in case of degeneration.
Risks for BE are longstanding disease, erosive
esophagitis, advanced age, male gender, obesity,
smoking, hiatal hernia [37], and peptic strictures
(triplicate the risk).
Identifying patients with BE on the basis of
symptoms only is impossible, and this weak clinical correlation hampers BE’s early diagnosis and
monitoring.
The true prevalence of BE is not known, but
this condition is estimated to affect 1.6
general population,
alarming 159
% increase from 1993 to
with rising incidence: an
in fact been observed [37]. BE is detected in 3
% of the
2005 has
%
of patients who have had GERD for less than 1
year and in more than 20 % of those who had
symptoms for 10 years [65].
Male to female
ratio for BE is 3:1, and the average patients’ age is 55 years. BE does not cause
symptoms per se, but it carries a substantial risk
of progression to adenocarcinoma each year.
The gold standard for diagnosis is endoscopy
with biopsy. Since severe erosive esophagitis can
impair detection of BE, aggressive PPI therapy
should be administered in patients with known
esophagitis in order to heal the esophageal mucosa and maximize the diagnostic potential of
endoscopy [66]. It is advisable to perform an endoscopy to screen for BE in all patients with a
long history of disease (5–10 years) [67] or when
patients with GERD are >
endoscopy is positive, guidelines
50 years of age. If the
advise for an
endoscopic surveillance program at specific intervals according to their histological pattern
[30]:
Fig. 7.5 Endoscopic view of early-stage esophageal can-
cer arising in Barrett’s mucosa
Every 3–5 years if there
•
is no evidence of dys-
plasia;
Every 6 months for LGD;
•
• Every 3 months for HGD in patients not
receiving endoscopic or surgical therapy
If BE is nondysplastic, it has a 0.25
of progression to carcinoma each year
rises to 0.6
− 5 % in BE with LGD [68,
.
− 0.4 % risk
, which
69].
Both the American Gastroenterologic Association and the British Society of Gastroenterology acknowledge endoscopic radiofrequency
ablation (RFA) as the first line of treatment for
patients with HGD, but no data sustain its use in
BE with LGD and without dysplasia [70]. Complete eradication of metaplasia has been reported
to be persistent after 3 years in 91
with intestinal
metaplasia, in 96
% of patients
% of patients
with HGD, and in 100 % of those with LGD [70].
The
most worrisome consequence of BE ablation
is the persistence of disease within the submucosa covered by normal neosquamous epithelium:
the so-called “buried glands” phenomenon. This
event is rare but potentially dangerous since it is
difficult to monitor these glands for possible degeneration and there are reported cases of cancer
that arise underneath a normal squamous mucosa.
Endoscopic mucosal resection (EMR) is a
valid technique to better assess the presence of
cancer within an irregular esophageal mucosa
7.5) or even underneath a normal epithe-
(Fig.
lium. W
ith EMR, several centimeters of mucosal and submucosal layers can be removed, thus
allowing for precise staging of the lesion and
82 C. Barbon et al.
Fig. 7.6 Endoscopic view of advanced esophageal can-
cer
possible complete resection if no breach to the
deep layers of esophagus has occurred.
EMR is usually indicated for focal lesions, but
it can be associated with RFA for treatment of
broader BE areas, with an eradication rate of dysplasia and cancer ranging from 85 to 100 %. Additionally to being a valid option, this procedure
guarantees a better life quality, and less morbidity and mortality compared to esophagectomy.
When endoscopic therapy fails, in case of long
segments of BE with multifocal cancer, or when
the patient is noncompliant with the need for a
demanding endoscopic surveillance program,
esophagectomy should be considered.
Esophageal adenocarcinoma (Fig. 7.6) is the
most dreadful evolution of severe reflux disease.
Its incidence is rapidly increasing in the western
world, especially in white males, after the age of
50. The poor prognosis of this disease underlines
the importance of individuating and starting endoscopic surveillance in patients at risk. Patients
with BE have an overall 0.5 % yearly progression rate to esophageal adenocarcinoma [71], but
there is a 7 % yearly incidence in patients with
HGD [72].
No endoscopic screening is required for the
general population, but endoscopy should be
considered for patients with multiple risk factors,
such as age > 50, male gender, obesity, Caucasian
race, chronic GERD, and hiatal hernia [68,73].
Early detection of cancer decreases mortality and
increases options for treatment. The mainstay of
therapies for locally advanced esophageal adeno-
carcinoma is neo-adjuvant therapy followed by
esophagectomy. Endoscopic mucosal and submucosal resection, possibly combined with RFA,
should be considered for early stages with good
prognosis [74].
Conclusion
Severe reflux esophagitis is a disease characterized by a broad-spectrum presentation. It can be
kept under control with several therapeutic strategies, but if not properly addressed, it may progress to severe complications.
Five Key Points on How to Avoid Complications
• Do not overlook symptomatology; always
consider reflux esophagitis in the differential
diagnosis of upper GI manifestation, especially in patients with long history of GERD.
• Once the disease is diagnosed, esophagitis
should be graded according to the Los Angeles criteria and risk factors assessed; when
necessary, the patients should be monitored.
• Administer appropriate and targeted medical
therapy and check for its efficacy and patients’
compliance.
• Appropriately select patients who are ideal
candidates for surgery and target the surgical
technique according to their characteristics.
• If the patient is a surgical candidate, consider
surgery early in the disease process before the
development of complications.
Five Key Points on Diagnosing and/ or Managing the Complications Either Intraoperatively or Postoperatively
• The best diagnostic technique to diagnose
complications is endoscopy associated with
biopsy to evaluate the presence of metaplasia
or dysplasia.
• EMR is the best tool for staging early esophageal cancer.
• Consider adding a fundoplication for refractory endoscopic treatment of GERD complications.
• Intraoperative assessment for the presence of
short esophagus is key for the success of ARS.
• Esophagectomy is a good option for the “unsalvageable” esophagus and offers patients’ good
long-term quality of life.
References
1. Kauer WK, Stein HJ. Emerging concepts of bile
reux in the constellation of gastroesophageal reux
disease. J Gastrointest Surg. 2010;14(Suppl 1):S9–
16. doi:10.1007/s11605-009-1014-4.
2. Dent J, El-Serag HB, Wallander
Epidemiology of gastro-oesophageal reux disease:
a systematic review. Gut. 2005;54:710–7.
3. Peery AF, Dellon ES, Lund J, et al. Burden of gastro-
intestinal
Gastroenterology. 2012;143:1179–87.
4. Bredenoord AJ1, Pandolno
Gastro-oesophageal reux disease. Lancet.
2013;381(9881):1933–42. doi:10.1016/S01406736(12)62171-0.
5. Society for Surgery of the Alimentary Tract. SSAT
patient care guidelines. Surgical treatment of reux
esophagitis. J Gastrointest Surg. 2007;11(9):1207–9.
6. Liu JJ, Saltzman JR. Management of gastroesopha-
geal reux disease. South Med J. 2006;99(7):735–
41; quiz 742, 752.
7. Ronkainen J, Aro P
Lind T, Bolling-Sternevald E, et
of gastroesophagea
with or without symptoms in the general adult Swedish population: akalixanda study report. Scand J Gastroentero. 2005;40(3):275–85.
8. Carlsson R, Dent J, Watts R, et al. Gastro-oesopha-
geal
study of different treatment strategies with omeprazole. International GORD study group. Eur J Gastroenterol Hepatol. 1998;10:119–24.
9. Venables TL, Newland RD, Patel
zole 10 milligrams once daily, 20 milligrams once
daily, or ranitidine 150 milligrams twice daily, evaluated as initial therapy for the relief of symptoms of
gastro-oesophageal reux disease in general practice.
Scand J Gastroenterol. 1997;32:965–73.
10. Souza RF.
agitis and Barrett’s metaplasia. Biochem Soc Trans.
2010;38(2):348–52. doi:10.1042/BST0380348.
Desai KM, Frisella MM, Soper NJ.
11.
after laparoscopic antireux surgery in patients with
and without preoperative endoscopic esophagitis.
J Gastrointest Surg. 2003;7(1):44–51.Discussion
51–2.
disease in the United States: 2012 update.
, Storskrubb T, Johansson SE,
l reux symptoms and esophagitis
reux disease in primary care: an international
The role of acid and bile reflux in oesoph-
MA, Johansson S.
JE, Smout AJ.
al. High prevalence
al. Omepra-
AC, et
Clinical outcomes
837 Severe Reflux-Induced Esophagitis
Lundell LR, Dent J, Bennett JR, Blum AL, Arm-
12.
strong D, Galmiche JP, Johnson F, Hongo M, Richter
JE, Spechler SJ, Tytgat GN, Wallin L. Endoscopic
assessment of oesophagitis: clinical and functional
correlates and further validation of the Los Angeles
classication. Gut. 1999;45:172–80.
13. Genta RM, Spechler SJ, Kielhorn AF. The Los Angeles and Savary-Miller systems for grading esophagitis: utilization and correlation with histology. Dis
Esophagus. 2011;24(1):10–7.
14.
Westhoff B, Brotze S,
Cherian R, Mayo MS, etal. The frequency of Barrett’s esophagus in high-risk patients with chronic
GORD. Gastrointest Endosc. 2005;61(2):226–31.
Labenz J, Nocon M, Lind T
15.
D, Meyer-Sabellek W, etal. Prospective follow-up
data from the ProGORD study suggest that GORD
is not a categorical disease. Am J Gastroenterol.
2006;101(11):2457–62.
16. Orr WC. Review article: sleep-related gastro-oesophageal reux as a distinct clinical entity. Aliment Pharmacol Ther. 2010;31:47–56.
17. Lagergren J, Bergstrom R, Lindgren A, Nyren O.
Symptomatic gastroesophageal reux as a risk factor
for esophageal adenocarcinoma. N Engl J Med.
1999;340:825–31.
Armstrong D, Marshall JK, Chiba N, et al. Canadian
18.
consensus conference on the management
esophageal reux dis-ease in adults—update 2004.
Can J Gastroenterol. 2005;19:15–35.
19. Vakil N, Moayyedi P, Fennerty MB, et al. Limited
value of alarm features in the diagnosis of upper
gastrointestinal malignancy: systematic review and
meta-analysis. Gastroenterology. 2006;131:390–401.
20. Rantanen TK, Sihvo EI, Rasanen JV, et al. Gas-
troesophageal
is increasing: analysis of fatal cases after medical and surgical treatment. Am J Gastroenterol.
2007;102:246–53.
GralnekI M, Dulai GS, Fennerty MB, et al. Esome-
21.
prazole
esophagitis: a meta-analysis of randomized clinical
trials. Clin Gastroenterol Hepatol. 2006;4:1452–8.
Vela MF, Camacho-Lobato
22.
Simultaneous intraesophageal impedance and pH
measurement of acid and nonacid gastroesopha-
geal reux: effect of omeprazole. Gastroenterology.
2001;120:1599–606.
23.
Stein HJ, Kauer WKH, Feussner H, et al. Bile acids
as components of the duodenogastric reuxate:
detection, relationship to bilirubin, mechanism of
injury and clinical relevance. Hepato.Gastroenterol.
1999;46:66–7.
24. Kauer WKH, Burdiles P
denal
juice reux into the esophagus of patients with
complicated GERD. Am J Surg. 1995;169:98–104.
Stein HJ, Kauer
25.
in benign and mali
of medical acid suppression and fundoplication. J
Gastrointest Surg. 1998;2:233–41.
reux disease as a cause of death
versus other proton pump inhibitors in erosive
Weston A, McElhinney C,
, Leodolter A, Jaspersen
of gastro-
L, Srinivasan R, et
, Ireland A, et
WKH, Feussner H, et
gnant Barrett’s esophagus. Effect
al. Does duo-
al. Bile reux
al.
84 C. Barbon et al.
40.
26. Kaltenbach T, Crockett S, Gerson LB. Are lifestyle
measures effective in patients with gastroesophageal
reux disease? An evidence-based approach. Arch
Intern Med. 2006;166:965–71
27.
Kahrilas PJ, Shaheen NJ,
Vaezi MF. American gastroenterological association institute technical review
on the management of gastroesophageal reux disease. Gastroenterology. 2008;135:1392–413.
28.
Tytgat GNJ. Review
article: management of mild and
severe gastro-oesophageal reux disease. Aliment
Pharmacol Ther. 2003; 17(Suppl 2):52–6.
29. Chubineh S
1
, Birk J. Proton pump inhibitors:
the good, the bad, and the unwanted. South
Med J. 2012;105(11):613–8. doi:10.1097/
SMJ.0b013e31826efbea.
30.
Spechler SJ, Sharma P
, Souza RF, Inadomi JM,
Shaheen NJ. American gastroenterological association medical position statement on the management of Barrett’s esophagus. Gastroenterology.
2011;140(3):1084–91.
31.
Vela MF, Camacho-Lobato
Intraesophageal impedance
L, Srinivasan R, et
al.
and pH measurement of
acid and non-acid reux: effect of omeprazole. Gastroenterology. 2001;120:1599–606.
32.
Ghatak S, Reveiller M, T
oia L, Ivanov A, Godfrey
TE, Peters JH. Bile acid at low pH reduces squamous differentiation and activates EGFR signaling
in esophageal squamous cells in 3-D culture. J Gastrointest Surg. 2013;17(10):1723–31. doi:10.1007/
s11605-013-2287-1.
33.
Kahrilas PJ
1
, Shaheen NJ, Vaezi MF. American gastroenterological association institute technical review
on the management of gastroesophageal reux disease. Gastroenterology. 2008;135(4):1392–1413,
1413.e1–5. doi:10.1053/j.gastro.2008.08.044.
Bavishi C, Dupont HL. Systematic review:
34.
the use
of proton pump inhibitors and increased susceptibility to enteric infection. Aliment Pharmacol Ther.
2011;34:1269–81.
Laheij RJ, Sturkenboom MC, Hassing JR, et al. Risk
35.
of community-
acquired pneumonia and use of gas-
tric acid-suppressive drugs. JAMA. 2004;292:1955–
60.
36. Campos GM
1
, Peters JH, DeMeester TR, Oberg S,
Crookes PF, Tan S, DeMeester SR, Hagen JA, Bremner CG. Multivariate analysis of factors predicting
outcome after laparoscopic Nissen fundoplication. J
Gastrointest Surg. 1999;3(3):292–300.
37. Parasa S, Sharma P. Complications of gastro-
oesophageal reux disease. Best Pract Res Clin
Gastroenterol. 2013;27(3):433–42. doi:10.1016/j.
bpg.2013.07.002.
Galmiche JP, Hatlebakk J, Attwood S, et al. Laparo-
38.
scopic
antireux surgery vs esomeprazole treatment
for chronic GERD: the lotus randomized clinical
trial. JAMA. 2011;305:1969–77.
Parrilla P, Martinezde
39.
Haro LF, Ortiz A, et
al. Longterm results of a randomized prospective study comparing medical and surgical treatment of Barrett’s
esophagus. Ann Surg. 2003;237:291–8.
Gurski RR, Peters JH, Hagen JA, et al. Barrett’s
esophagus
can and does regress after antireux sur-
gery: a study of prevalence and predictive features. J
Am Coll Surg. 2003;196:706–12.
Zaninotto G, Parente P
41.
, Salvador R, et
al. Long-term
follow-up of Barrett’s epithelium: medical versus
antireux surgical therapy. J Gastrointest Surg.
2012;16:7–14.
42. Horvath KD, Jobe BA, Herron Dm, Swanstrom LL.
Laparoscopic toupet fundoplication is an inadequate
procedure for patients with severe reux disease. J
Gastrointest Surg. 1999;3:583–91.
43.
Patti MG, Robinson T
, Galvani C, Gorodner MV, Fisichella PM, Way LW. Total fundoplication is superior
to partial fundoplication even when esophageal peristalsis is weak. J Am Coll Surg. 2004;198:863–70.
44. Society for Surgery of the Alimentary Tract. SSAT
patient care guidelines. Management of Barrett’s
esophagus. J Gastrointest Surg. 2007;11(9):1213–5.
45. Broeders JA
1
, Draaisma WA, Bredenoord AJ, Smout
AJ, Broeders IA, Gooszen HG. Long-term outcome
of Nissen fundoplication in non-erosive and ero-
sive gastro-oesophageal reux disease. Br J Surg.
2010;97(6):845–52. doi:10.1002/bjs.7023.
Braghetto I
46.
1
, Csendes A, Burdiles P, Botero F, Korn
O. Results of surgical treatment for recurrent post-
operative gastroesophageal reux. Dis Esophagus.
2002;15(4):315–22.
Catarci M, Gentileschi P
47.
R, Gaspari AL, et
, Papi C, Carrara A, Marrese
al. Evidence-based appraisal
antireux fundoplication. Ann Surg. 2004;239:325–
37.
Grant AM, Cotton SC, Boachie C, Ramsay CR, Kru
48.
kowski ZH, Heading RC, Campbell MK. Minimal
access surgery compared with medical management
for gastro-oesophageal reux disease: ve year follow-up of a randomised controlled trial (REFLUX).
BMJ. 2013;346:f1908. doi:10.1136/bmj.f1908.
49. Faria R, Bojke L, Epstein D, Corbacho B, Sculpher
M.REFLUX trial group. Cost-effectiveness of laparoscopic fundoplication versus continued medical
management for the treatment of gastro-oesophageal
reux disease based on long-term follow-up of the
REFLUX trial. Br J Surg. 2013;100(9):1205–13.
50. Rossi M
1
, Barreca M, deBortoli N, Renzi C, Santi
S, Gennai A, Bellini M, Costa F, Conio M, Marchi
S. Efcacy of Nissen fundoplication versus medical
therapy in the regression of low grade dysplasia in
patients with Barrett esophagus: a prospective study.
Ann Surg. 2006;243(1):58–63.
51. Lipham JC, Demeester TR, Ganz RA, et al. â£e
LINX(®) reux management system: conrmed
safety and efcacy now at 4
years. Surg
Endosc.
2012;26:2944–9.
Locke GR, Horwhat J, Mashimo H, Savarino
52.
Zentilin P, Savarino V, Zerbib F, Armbruster SP,
Wong RK, Moawad F. Endotherapy for and tailored
approaches to treating GERD, and refractory GERD.
Ann N Y Acad Sci. 2013;1300:166–86. doi:10.1111/
nyas.12240.
of
-
E,
857 Severe Reflux-Induced Esophagitis
53. Pisegna J, Holtmann G, Howden CW, Katelaris PH,
Sharma P, Spechler S, Triadalopoulos G, Tytgat G.
Review article: oesophageal complications and con-
sequences of persistent gastro-oesophageal reux
disease. Aliment Pharmacol Ther. 2004; 20(Suppl
9):47–56.
54.
Awad ZT
1
, Filipi CJ, Mittal SK, Roth TA, Marsh
RE, Shiino Y, Tomonaga T. Left side thoracoscopically assisted gastroplasty: a new technique for
managing the shortened esophagus. Surg Endosc.
2000;14(5):508–12.
55.
Urbach DR, Khajanchee YS, Glasgow RE,
Hansen
PD, Swan-strom LL. Preoperative determinations
of an esophageal-length-ening procedure in laparo-
scopic antireux surgery. Surg Endosc.
56.
Pregun I, Hritz I, Tulassay Z, Herszényi L. Peptic
esophageal stricture:
medical treatment. Dig Dis.
2009;27(1):31–7. doi:10.1159/000210101. Epub
2009 May 8. Review.
57.
Spechler SJ. Clinical manifesta
tions and esophageal complications of GORD. Am J Med Sci.
2003;326(5):279–84.
58.
Braghetto I, Csendes
A, Burdiles P, Korn O, Compan
A, Guerra JF. Barrett’s esophagus complicated with
stricture: correlation be-tween classication and the
results of the different therapeutic options. World J
Surg. 2002;26:1228–33.
59.
Ferguson DD. Evaluation
and management of
benign esophageal strictures. Dis Esophagus.
2005;18(6):359–64.
60.
Dakkak M, Hoare RC, Maslin SC, et al. Oesophagitis
is as important as oesophageal
stricture diameter in
determining dysphagia. Gut.1993;34:152–5.
61.
Watson A.
Reux stricture of the oesophagus. Br J
Surg. 1987;74:443–8.
62.
Kochhar R, Ray JD, Sriram
PV, Kumar S, Singh K.
Intralesional steroids augment the effects of endoscopic dilation in corrosive esophageal strictures.
Gastrointest Endosc. 1999;49(4 Pt 1):509–13.
63.
Bender EM, Walbaum PR. Esophagogastrectomy
for
benign esophageal stricture. Fate of the esophagogastric anastomosis. Ann Surg. 1987;205:385–8.
64.
Buttar NS, Falk GW. Pathogenesis of gastroesopha
geal reux and Barrett esophagus. Mayo Clin Proc.
2001;76:226–34.
65.
Lieberman DA, Oehlke M, Helfand
M. Risk factors
for Barrett’s esophagus in community-based practice. Gorge consortium. Gastroenterology outcomes
research group in endoscopy. Am J Gastroenterol.
1997;92:1293–7.
66. Modiano N, Gerson LB. Risk factors for the detection of Barrett’s esophagus in patients with erosive
esophagitis. Gastrointest Endosc. 2009;69(6):1014–
20. doi:10.1016/j.gie.2008.07.024.
67.
Inadomi JM, Sampliner R, Lagergren J, et al. Screen-
ing and surveillance
for Barrett esophagus in high
risk groups: a cost-utility analysis. Ann Intern Med.
2003;138:176–86.
68.
Prasad GA, Bansal A, Sharma
P, Wang KK. Predictors of progression in Barrett’s esophagus: current
knowledge and future directions. Am J Gastroentero.
2010;105(7):1490–502.
69.
Leodolter A, Nocon M, V
Richter K, et
metaplasia
al. Progression of specialized intestinal
at the cardia to macroscopically evident
ieth M, Lind T, Jaspersen D,
Barrett’s esophagus: an entity of concern in the Progord study. Scand J Gastroentero. 2012;47(12):1429–
35.
70. Shaheen NJ, Sharma P, Overholt BF, et al. Radiofrequency ablation in Barrett’
s esophagus with dyspla-
sia. N Engl J Med. 2009;360:2277–88.
71.
Shaheen NJ, Crosby MA, Bozymski EM, et al.
Is there publication bias in the reporting
risk in Barrett’s esophagus?.Gastroenterology.
2000;119:333–8.
72.
Rastogi A, Puli S, El-Serag HB, et al. Incidence of
esophageal
adenocarcinoma in patients with Barrett's
esophagus and high-grade dysplasia: a meta-analysis. Gastrointest Endosc. 2008;67:394–8.
73.
Falk GW, Jacobson BC, Riddell RH, Rubenstein
El-Zimaity H, Drewes AM, et
al. Barrett’s esopha
gus: prevalence- incidence and etiology-origins. Ann
N Y Acad Sci. 2011;1232:1–17.
74.
Mori H
1
, Kobara H, Fujihara S, Nishiyama N,
Nomura T, Kobayashi M, Hagiike M, Izuishi K,
Suzuki Y, Masaki T. Simultaneous resection of
Barrett’s esophageal cancer and severe stenosis
-
caused by reux esophagitis. Gastrointest Endosc.
2012;76(3):689–90. doi:10.1016/j.gie.2011.08.035.
of cancer
JH,
-