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322 Part III Esophagus
Yield pressure (mm Hg)
40
36
32
28
24
20
16
12
8
4
0
FIGURE 15-2 Yield pressure of the lower esophageal sphincter
decreases as hiatal hernia size increases.
No hernia <3 cm hernia 3 cm hernia
†
*
diaphragm. 17 Additionally, normal pressure of the GEJ from
manometric tracings has been shown to range from 15 ± 11
mm Hg at the end of expiration to 40 ± 13 mm Hg at the
end of inspiration mainly as a result of the diaphragmatic
18
contribution.
is pinchcock action of the diaphragm is
particularly important as a protection mechanism against
re ux induced by sudden increases in intra-abdominal
19
pressure.
is mechanism is obviously disrupted by the
presence of a hiatal hernia where the intrinsic LES has
“migrated” proximal to the diaphragmatic pinch.
Stomach
Impaired function of the stomach such as abnormal gastric
emptying may contribute to GERD by increasing intragas-
20
tric pressure, distension, and LES unrolling.
is may occur
in patients with a large hiatal hernia, in which the herniated
stomach in the chest does not empty appropriately, gastric
outlet obstruction either from malignancy or peptic ulcer
disease, and diabetic gastroparesis.
COMPLICATIONS OF GERD
e complications of GERD result from the damage in icted
by gastric juice on the esophageal mucosa, pharyngeal or
respiratory epithelium, and the mucosal changes caused by
their subsequent repair and brosis. ese complications
can be categorized into three groups: (1) mucosal complications such as esophagitis or stricture; (2) extraesophageal
TABLE 15-3: COMPLICATIONS OF
GASTROESOPHAGEAL REFLUX DISEASE:
150 CONSECUTIVE CASES WITH PROVEN
GASTROESOPHAGEAL REFLUX DISEASE
(24-HOUR ESOPHAGEAL pH MONITORING,
ENDOSCOPY, AND MOTILITY)
Structurally
Complication No.
None 59 58 42
Erosive esophagitis 47 23 77
Stricture 19 11 89
Barrett’s esophagus 25 0 100
Total 150
a Grade more severe with defective cardia.
Reproduced, with permission, from DeMeester TR. Gastroesophageal re ux
disease. In: Moody FG, Carey LC, Scott Jone R, et al, eds. Surgical Treatment of
Digestive Disease . Chicago, IL: Year Book Medical; 1990:81.
Normal
Sphincter (%)
Structurally
Defective
Sphincter (%)
a
or respiratory complications such as laryngitis, pneumonia,
asthma, and pulmonary brosis; and (3) metaplastic and neoplastic complications such as Barrett’s esophagus and adenocarcinoma. e prevalence and severity of GERD- related
complications are positively correlated with the degree of LES
dysfunction and impaired esophageal motility ( Table 15-3 ).
21
Mucosal Complications
Mucosal complications such as esophagitis and stricture
can occur in the presence of two predisposing factors: (1)
a mechanically defective LES and (2) an increased esophageal exposure to the gastric uid with a pH less than 4 and
greater than 7 ( Fig. 15-3 ).
gastric uid can include acid and pepsin as well as biliary and
pancreatic secretions that travel from the duodenum into the
22,
stomach.
23 Although acid and activated pepsin are the key
ingredients of the gastric juice that leads to esophagitis, it has
been established that the most severe epithelial injury occurs
during exposure to bile salts combined with acid and pep-
24
Previous experimental studies have shown that gastric
sin.
or duodenal juice alone causes minimal or little damage to the
esophageal mucosa, but the combination of duodenal juice
and gastric juice is highly noxious. Previous study to directly
measure esophageal bilirubin exposure as a marker of duodenogastroesophageal re ux has shown that 58% of patients
with GERD have increased esophageal exposure to duodenal
juice and that this exposure occurs most commonly when
the esophageal pH is between 4 and 7 ( Fig. 15-4 ).
this pH range, there is formation of nonpolarized, soluble
bile acids, which can di use through the cell membrane and
cause damage to the mucosal cells. Additionally, this type
of exposure correlates with the development of Barrett’s
esophagus ( Fig. 15-5 ).
21
e components of the re uxed
25
Within
25
e fact that the combination of
Chapter 15 Gastroesophageal Reux Disease and Hiatal Hernia (Including Paraesophageal) 323
Percent
Prevalence
*
% Total time
Prevalance of Patients With Increased Bilirubin
30%
25%
20%
15%
10%
5%
0%
% Time pH <4
% Time pH >7
Volunteers No GERD GERD
No complic.
@
GERD
Esophag.
@
GERD
Stricture
*
GERD
Barrett’s
FIGURE 15-3 Esophageal acid and alkaline exposure expressed as
percentage of total time pH of less than 4 and more than 7. * = p <.01
versus gastroesophageal reux disease patients with no complication. @ =
p < .05 versus gastroesophageal reux disease patients with no complica-
tions. (Reproduced from Stein HG, Barlow AP, DeMeester TR, Hinder
RA. Complications of gastroesophageal reux disease: role of the lower
esophageal sphincter, esophageal acid and acid/ alkaline exposure, and
duodenogastric reux. Ann Surg. 1992;216:39.)
100
80
60
40
20
0
Normal
subjects
n = 25
**
No mucosal
injury
n = 16
**
Erosive
esophagitis
n = 10
*
Barrett’s
esophagus
n = 27
FIGURE 15-5 Prevalence of abnormal esophageal bilirubin exposure
in healthy subjects and in patients with gastroesophageal reux disease
with varied degrees of mucosal injury. (* p < .03 vs all other groups, **
p < .3 vs healthy subjects.) (Reproduced from Kauer WK, Peters JH,
DeMeester TR, et al. Mixed reux of gastric juice is more harmful to
the esophagus than gastric juice alone: the need for surgical therapy
reemphasized. Ann Surg. 1995;222:525.)
70
60
50
40
30
20
10
0
% Time
20
15
10
5
0
Gastric reflux
(n = 22)
pH
<4
A
B
pH
4–7
Mixed reflux
(n = 31)
pH
>7
FIGURE 15-4 A. Prevalence of reux types in 53 patients with
gastroesophageal reux disease. B. Esophageal luminal pH during
bilirubin exposure. (Reproduced from Kauer WK, Peters JH,
DeMeester TR, et al. Mixed reux of gastric juice is more harmful to
the esophagus than gastric juice alone: the need for surgical therapy
reemphasized. Ann Surg. 1995;222:525.)
gastric and duodenal juice is more noxious to the esophageal
mucosa than gastric juice alone may provide an explanation
for the observation that 25% of patients with reux esophagitis develop recurrent and/or progressive mucosal damage
21
despite medical therapy.
Clinically, there is poor correla-
tion between the symptom of heartburn and the endoscopic
26
nding of esophagitis.
e reux of acidic gastric juice
combined with duodenal contents can irritate nerve endings
close to the luminal surface and cause severe heartburn in
the absence of endoscopically detectable erosions; bile salts
inhibit pepsin and acid inactivates trypsin, and the patient
exhibits little or no gross evidence of esophagitis. By contrast, the reux of alkaline gastric juice may occur without
symptoms because of the absence of hydrogen ions but cause
endoscopically evident esophagitis secondary to bile-activated trypsin exposure to the esophageal epithelium. is is
supported by recent clinical studies that demonstrated that
the presence of alkaline reux is associated with the devel-
25,27
opment of mucosal injury.
using either prolonged ambulatory aspiration techniques
or spectrophotometric bilirubin measurement
In addition, several studies
28
29
have shown
that patients with GERD have more concentrated bile acid
exposure to the esophageal mucosa than normal subjects,
commonly in the supine position during sleep and in the
upright position during the postprandial period. Furthermore, reux of both acid and pancreaticobiliary juice is the
most prevalent pattern of exposure and present in 100% of
complicated Barrett’s patients, 89% of uncomplicated Barrett’s patients, 79% of patients with esophagitis, and 50%
30,31
of patients with NERD.
ese ndings support that the
reux of duodenal juice containing bile acids is common in
324 Part III Esophagus
patients with GERD and that proton pump inhibitor (PPI)
therapy cannot prevent mucosal damage due to bile acids.
Esophageal stricture (circumferential scarring) formation and/or shortening (axial scarring) can be associated
with severe esophagitis or Barrett’s esophagus. Scarring
occurs at the site of maximal inammatory injury (ie,
squamocolumnar junction). ought by some to be a protective mechanism, the metaplastic columnar epithelium
advances proximally into the area of inammation leading to
“protection” of that given length of esophagus; the proximal
migration of the squamocolumnar junction leads to more
proximal stricture formation within the esophagus. e presence of stricture can be an indicator of GERD even if there
is no evidence of esophagitis or Barrett’s esophagus. However, in patients with normal acid exposure, the stricture may
be due to malignancy or a drug-induced chemical injury.
32
Biopsy should be obtained to exclude malignancy. A short
esophagus should be suspected when there is a hiatal hernia
of greater than 5 cm that does not reduce in the upright
position on esophogram.
Extraesophageal or Pulmonary
Complications
It has been increasingly recognized that a signicant proportion of patients with GERD have laryngeal or respiratory
symptoms such as cough, recurrent pneumonia, asthma, and
progressive pulmonary brosis, sometimes in conjunction
with typical GERD symptoms such as heartburn and regurgi-
33
tation.
the development of lung disease such as asthma and idiopathic
pulmonary brosis has been established. Previous studies have
demonstrated that up to 50% of asthmatics have either endoscopic evidence of esophagitis or increased esophageal acid
exposure on 24-hour ambulatory pH monitoring,
that 87% of patients with idiopathic pulmonary brosis
90.9% with cystic brosis
on esophageal pH monitoring.
of reux-induced respiratory symptoms: (1) aspiration of
gastric contents and (2) vagally mediated bronchoconstriction.
Recent clinical studies have demonstrated a strong correlation
between idiopathic pulmonary brosis and hiatal hernia and
a high association between GERD and pulmonary disease
such as asthma.
mal esophagus is often identied in patients with respiratory
symptoms and GERD. Scintigraphic studies have demonstrated aspiration of ingested radioisotope in patients with
GERD and respiratory symptoms.
and esophageal pH monitoring has demonstrated the presence of concomitant acidication both in the trachea and
the esophagus in patients with asthma.
shown an increased airway resistance after the instillation of
hydrochloric acid into the trachea.
known that bronchoconstriction occurs following the acid
exposure in the distal esophagus.
In addition, a strong association between GERD and
34,35
and
36
37
have documented GERD based
and
Two mechanisms have been proposed as the pathogenesis
33
Pathological acid exposure in the proxi-
38
Simultaneous tracheal
39
Animal studies have
40
Additionally, it is well
41
is can be explained by
the common embryologic origin of the trachea and esophagus and their shared vagal innervation.
It is dicult to document that respiratory symptoms and/
or injury are caused the underlining GERD as both are very
prevalent. In a substantial number of patients with reuxinduced respiratory symptoms, GERD is often silent and is
only uncovered when investigation is initiated. A high index
of suspicion is required, especially in patients with poorly
controlled adult-onset asthma in spite of appropriate bronchodilator therapy. Objective esophageal testing should be
performed to document evidence of GERD and to attempt to
correlate extraesophageal symptoms with reux events. Upper
endoscopy may reveal the presence of esophagitis or Barrett’s
esophagus. Manometry may demonstrate a hypotensive LES
or some degree of impaired esophageal motility. Traditionally, the diagnosis of reux-induced respiratory symptoms
has been made using ambulatory dual probe pH monitoring;
one probe is positioned within the distal esophagus and the
other at a proximal location such as the trachea, pharynx,
or proximal esophagus. Although ambulatory esophageal pH
monitoring allows a direct correlation between esophageal
acidication and respiratory symptoms, the chronological
relationship between reux events and bronchoconstriction is
complex. e sensitivity of this approach is poor as much of
the acid exposure is neutralized proximally after mixing with
saliva. Multichannel intraluminal impedance-pH (MII-pH)
has been introduced as a promising tool to evaluate the extension of reux and its symptom correlation regardless of the
composition of reuxate (liquid, gas, mixed, alkaline, acidic),
especially in patients with atypical symptoms. Although several studies have shown that combined 24-hour MII-pH has a
high yield for detection of GERD with atypical symptoms,
the clinical utility of MII-pH is still being investigated.
Once GERD is suspected or thought to be responsible for
respiratory symptoms, the treatment options may be either
the trial of high-dose PPI therapy (BID or TID dosing)
or antireux surgery. A 3–6 months trial of high-dose PPI
therapy may suggest that GERD is partly or completely
responsible for the development of respiratory symptoms.
However, the persistence of symptoms despite the maximal
PPI therapy does not necessarily rule out the possible contribution of GERD. e algorithm depicted in Fig. 15-6 is
made based on the outcome of dual-probe 24-hour pH monitoring and esophageal manometry in patients with respiratory symptoms and does not include impedance. Previous
studies have demonstrated that acid suppressive therapy
with PPI improves asthma symptoms and/or peak expiratory
ow rates in up to 73% of asthmatics with GERD, although
fewer than 15% can be expected to have objective improvements in their pulmonary function parameters.
studies were conducted with a relatively short course of acid
suppressive therapy (<3 months). is time period may have
been sucient for symptomatic improvement but insucient for recovery of pulmonary function. Given the fact that
acid suppressive therapy can only reduce the acidity of the
gastric uid but does not reduce the total number of reux
events, the conicting results regarding medical therapy in
4,42,43
27
Most
Chapter 15 Gastroesophageal Reux Disease and Hiatal Hernia (Including Paraesophageal) 325
24-hour Esophageal pH Monitoring
Proximal probe 1 cm below UES
Distal probe 5 cm above LES
pH negative,
no symptoms or symptoms
occurring with no change
of pH recorded in proximal
or distal probe
Tr ial of high dose PPI
No antireflux therapy
FIGURE 15-6 Correlation of symptoms with pH measurements predicts the likelihood that reux symptoms are caused directly by acid reux.
asthmatics may be secondary to the continued exposure of
the aerodigestive tract by caustic nonacid gastric juice. is is
supported by the literature indicating that antireux surgery
improves respiratory symptoms in nearly 90% of children
and 70% of adults with asthma and GERD.
ally, improvements in pulmonary function were observed in
around one-third of patients. A randomized controlled trial
to compare surgical treatment with medical treatment for
asthmatics with GERD demonstrated that fundoplication is
the most eective approach to improve asthma symptoms
and clinical course, although there was a minimal eect on
No symptoms or symptoms
occurring with no change
of pH recorded in proximal
probe but abnormal acid
exposure recorded in distal
Respiratory symptoms
35,44
Addition-
probe
likely due to GERD
indenite for dysplasia, (3) low-grade dysplasia (LGD), and
(4) high-grade dysphagia (HGD). Recent studies have identied a high prevalence of biopsy-proven intestinal metaplasia
at an endoscopically normal appearing GEJ, which is termed
cardia intestinal metaplasia (CIM). e signicance and natural history of CIM remains unknown. However, CIM is currently considered a separate entity from BE, although the
pathogenesis of CIM has been shown to be similar to reuxinduced BE.
include abnormal bile reux, hiatal hernia larger than 4 cm, a
defective LES, and esophageal motility disorder.
Symptoms and the recording
in the proximal probe of >7
episodes of a pH drop to >4 or
% time pH <4 >1
Abnormal motility
Low probability of
relief of symptoms
with surgery
55
Factors associated with the development of BE
Normal motility
High probability of
relief of symptoms
with surgery
56
pulmonary function, pulmonary medication requirement,
35
or survival.
reux surgery is to stabilize or delay the progression of endstage lung disease such as idiopathic pulmonary brosis.
On the other hand, a potential benet of anti-
45
Pathophysiology of Barrett’s Metaplasia
Metaplastic (Barrett’s esophagus)
and Neoplastic (Adenocarcinoma)
Complications
Barrett’s esophagus (BE) is dened as a columnar lined segment of esophagus of any length visible on endoscopy with
a biopsy showing intestinal metaplasia with the presence of
goblet cells (Fig. 15-7). Despite this classication, it is common to make the distinction between short-segment BE (<3
cm) and long- segment BE (≥3cm). Both short- and long-segment BE are considered pathologic and premalignant. e
prevalence of BE in the general population has been reported
to be 1–25%.
and carries a 30- to 50-fold increased risk of developing
esophageal adenocarcinoma via the metaplasia-dysplasia-carcinoma sequence compared to people without BE.
dence of esophageal adenocarcinoma in patient with known
BE may be as high as 0.5% per year.
sied into four broad categories: (1) BE without dysplasia, (2)
46–50
BE represents an end-stage form of GERD
51
e inci-
52–54
BE is currently clas-
e pathogenesis of BE begins with injury to the squamous epithelium of the distal esophagus, secondary to the
repeated distension of the stomach with large volume fatty
meals that result in eacement of the LES and exposure of
the distal esophageal squamous epithelium to caustic gastric
10
Continuous inammatory injury in this area of the
juice.
lower esophagus can cause permanent loss of the musculature of the LES, resulting in a mechanically defective LES.
With further loss of the gastroesophageal barrier function,
esophageal exposure worsens with resultant injury to progressively greater lengths of the squamous mucosa. Endoscopically, this injury can be observed as erosive esophagitis. e
resulting columnar metaplasia that develops in a previous
squamous-lined esophagus appears as a layer of mucus secreting columnar cells termed cardiac mucosa, which is a highly
specic mucosa that arises to replace injured squamous epithelium and is believed to be an adaptive response to better
57
tolerate exposure to gastric juice.
Eventually, cardiac mucosa
can remain without changing, form parietal cells, or develop
goblet cells to become intestinalized cardiac mucosa in the
divergent dierentiation pathways.
58
326 Part III Esophagus
remains controversial because of the lack of randomized
trials supporting its value.
60
However, previous retrospective studies have demonstrated that survival is statistically
enhanced if cancer is detected by endoscopic surveillance
61,62
rather than presenting with symptoms of obstruction.
Surveillance endoscopy should be performed in patients
with documented BE and those who have reux symptoms controlled with antisecretory therapy or antireux
surgery. e Seattle Protocol (biopsies with jumbo forceps
in four quadrants, along every centimeter of metaplastic
epithelium with extra biopsies taken from suspicious areas)
has been widely accepted. It should be noted that these
surveillance biopsies sample only a small fraction of the
esophageal epithelium (possibility for sampling error) but
63
are the only method available for recognizing dysplasia.
In patients with BE without dysplasia, we perform surveillance endoscopy every 3 years. e nding of low-grade
dysplasia (LGD) requires a follow-up endoscopy within 6
months to ensure that more advanced disease is not present. If the 6-month surveillance is negative for high-grade
dysplasia (HGD) or adenocarcinoma, yearly endoscopy is
performed until no dysplasia is present on two consecutive
A
annual endoscopies. e presence of HGD in at mucosa
should be conrmed by two experienced gastrointestinal
pathologists and a subsequent endoscopy is performed
within 3 months to reduce the chances of sampling error.
Nodules within a eld of HGD should undergo endoscopic
resection to rule out malignancy. Patients with conrmed
HGD should be counseled regarding the treatment options,
including intensive surveillance, ablation therapies, and
esophagectomy. Because the risk for the development of
invasive cancer is 50% within 3 years of diagnosis, HGD
is considered the threshold for therapeutic intervention.
Patients with LGD or no dysplasia can also be a candidate
for therapeutic intervention if they have excessive fear of
the development of cancer or a signicant family history
of BE and esophageal cancer. In our practice, patients with
nondysplastic BE who undergo antireux surgery are also
oered ablation of the involved segment of the esophagus.
B
FIGURE 15-7 Barrett’s esophagus. A. Endoscopic appearance.
B. Microscopic ndings.
Screening and Surveillance
Although patients with the highest likelihood of BE are
older (>50 years of age) Caucasian men with chronic reux
symptom,
of the inability to predict who has BE prior to endoscopy,
the lack of evidence-based criteria, the invasiveness and
expense of standard sedated endoscopy, and the increasing documentation of a subgroup of patients with BE
who lack reux symptoms.
59
screening for BE remains controversial because
60
Surveillance endoscopy also
Management of Dysplastic BE
Given the fact that HGD has a high rate of progression to
cancer and the prevalence of occult cancer in esophagectomy specimens of patients with a preoperative diagnosis of
only HGD has been reported to be 38–73%,
gectomy has been recommended as a standard of care for
HGD. However, esophagectomy is associated with signicant mortality and morbidity even in experienced cen-
67–69
ters.
Additionally, esophagectomy may be unnecessary
in the treatment of HGD because lymph node metastasis
70–72
is unlikely (<5%).
In the recently updated guidelines
by the American College of Gastroenterology, the authors
state that “esophagectomy is no longer the necessary treat-
60
ment response to HGD.”
Several endoscopic ablation
therapies such as photodynamic therapy,
64–66
esopha-
73
radiofrequency
Chapter 15 Gastroesophageal Re ux Disease and Hiatal Hernia (Including Paraesophageal) 327
TABLE 15-4: RISK FACTORS TO
CONSIDER WHEN USING ENDOSCOPIC
MANAGEMENT OF ESOPHAGEAL
NEOPLASIA (BARRETT’S ESOPHAGUS
WITH DYSPLASIA AND T1A ESOPHAGEAL
ADENOCARCINOMA)
Concurrent Cancer or Progression to Invasive Cancer
Low-Risk High-Risk
Unifocal (limited or focal),
at HGD
Lymph Node Involvement
Low-Risk High-Risk
Type I, IIa <20 mm, IIb, IIc
<10 mm
Well or moderately
di erentiated adenocarcinoma
(grading G1/G2)
Lesions limited to the
mucosa (m)
No lymphovascular invasion Presence of lymphovascular
HGD, high-grade dysphagia.
Type I: polypoid type, II: at type, IIa: at, elevated, IIb: level with the mucosa,
IIc: slightly depressed, III: ulcerated type.
74
ablation therapy,
and cryotherapy,
Multifocal HGD, HGD with
nodules
Type I, II >30 mm, type III
Poorly di erentiated
adenocarcinoma (grading G3),
squamous cell carcinoma
Invasion into submucosal
layer (sm)
invasion
75,
76 and endoscopic
resection techniques such as endoscopic mucosal resec-
77
and submucosal dissection 78 have been introduced.
tion
When considering these endoscopic therapies, the accurate
clinical staging is critical to prevent an inappropriate endoscopic therapy on a patient with a high risk of invasive or
79
metastatic disease ( Table 15-4 ).
Currently, radiofrequency
ablation therapy has been most commonly used since the
results of a multicenter, sham-controlled trial was reported
80
( Fig. 15-8 ).
In this trial, 127 patients with dysplastic BE
were randomly assigned to treatment with radiofrequency
ablation or a sham procedure. In patients with LGD, complete eradication of dysplasia occurred in 90.5% of those
in the ablation group, as compared with 22.7% of those in
the control group ( p < .001). In patients with HGD, com-
plete eradication occurred in 81.0% of those in the ablation
group, as compared with 19% of those in the control group
( p < .001). e rate of complications such as stricture and
bleeding was 6%. is study demonstrated the safety and
high e cacy of radiofrequency ablation therapy for dysplastic BE. eoretically, antire ux surgery potentially prevents
81
the progression to dysplasia and adenocarcinoma.
However, there have been no prospective randomized controlled
studies documenting this supposition. Given the fact that
BE results from GERD, antire ux surgery should be considered once BE is successfully treated.
A
B
FIGURE 15-8 Radiofrequency ablation therapy. A. HALO
which is a balloon-based endoscopic ablation. B. HALO
which is a scope-mounted endoscopic ablation.
360
system,
90
system,
PREOPERATIVE ASSESSMENT
OF PATIENTS WITH GERD
e purpose of esophageal objective testing is to determine
if the patients’ symptoms are due to gastroesophageal re ux
events and to de ne the severity of GERD and esophageal
motility that will impact on the selection of the type of surgical therapy. e esophageal objective testing includes barium
esophagram, upper endoscopy, esophageal manometry, esophageal pH monitoring, and MII-pH. Gastric emptying studies
may be considered in patients with suspicious symptoms such
as bloating and nausea.
Barium Esophagram
e barium esophagram is a test that is used to evaluate the entire
anatomy of esophagus, including the esophageal body and both
sphincters. is test is used to document the presence and size
of a hiatal hernia, stricture severity and location, diverticula,
esophageal emptying, and the presence of gastroesophageal
re ux, both spontaneously and induced by provocative maneuvers. Esophageal motility can be assessed to some extent but
is not the mainstay. Although the nding of re ux during the
barium esophagram is thought by some to be a reliable indicator for GERD, the absence of roentgenographic evidence of
re ux does not exclude disease.
328 Part III Esophagus
Upper Endoscopy
Upper endoscopy is performed to examine the mucosa
from the esophagus to the second portion of duodenum
and biopsies can be obtained if necessary. Although only
40–60% of patients with GERD have endoscopic evidence
of esophagitis, upper endoscopy has an excellent specicity
for this diagnosis when erosions are present. Upper endoscopy may identify unexpected ndings such as BE, malignancy, a large hiatal hernia, eosinophilic esophagitis, and
Zenker’s diverticulum. e location of the diaphragmatic
crura, the anatomic GEJ, and the squamocolumnar junction should be recorded.
Esophagitis is one of indicators of the presence of GERD.
e severity of esophagitis is most commonly described by
the Los Angeles classication
presence of one or more mucosal breaks that are less than
or equal to 5 mm in length. LA grade B is dened by the
presence of one or more mucosal breaks that are longer
than 5mm. LA grade C represents a more advanced stage
where one or more mucosal breaks are continuous between
the tops of two or more mucosal folds, but that involve less
than 75% of the esophageal lumen circumference. LA grade
D classies one or more mucosal breaks bridging the tops
of folds and involving at least 75% of the esophageal lumen
circumference. Nonerosive esophagitis is dicult to reliably
recognize endoscopically and its presence may be conrmed
based on the microscopic ndings of mucosal inltration
with polymorphonuclear leukocytes (PMNs), lymphocytes,
eosinophils, and the recently described balloon cells.
e extension of the relatively high mucosal papillae and
hyperplasia of the basal zone are further evidence of mucosal injury. However, these microscopic ndings do not prove
the presence of increased exposure to gastric juice as they can
occur from other forms of injury.
Barrett’s esophagus is suspected endoscopically when the
squamocolumnar junction is located proximal to the anatomic GEJ, and the characteristic appearance of a “salmon
pink color” mucosa is encountered in the lower esophagus.
Multiple random biopsies should be performed, and the diagnosis of BE must be conrmed by the microscopic ndings
of columnar epithelium with intestinalization. To standardize the endoscopic ndings of BE, the Prague classication
system of circumferential (C) and maximal length (M) has
been proposed (Fig. 15-9).
marks of the squamocolumnar junction, the GEJ, the extent
of circumferential columnar lining, and the most proximal
extension of the columnar mucosa excluding islands to
determine the length of BE. However, proximal islands of
columnar lining and ultrashort BE (<1 cm) are not included
in this system. e presence of BE is diagnostic of GERD.
Particular attention must be paid to the squamocolumnar
junction, where a mass, ulcer, nodularity, or inammatory
tissue should be considered suspicious for malignancy and
requires biopsy. Nodules encountered in a eld of BE should
be removed with endoscopic resection for histologic examination and deep staging.
82
; LA grade A is dened by the
85
86
is system identies the land-
83,84
8
6
Maximal extent of
Distance (cm)
from GEJ
FIGURE 15-9 Prague classication system to standardize Barrett’s
esophagus (BE). Diagrammatic representation of endoscopic BE
showing an area classied as C2M5. C: extent of circumferential
metaplasia; M: maximal extent of the metaplasia (C plus a distal
“tongue” of 3 cm). (Reproduced from Sharma P, Dent J, Armstrong
D, et al. e development and validation of an endoscopic grading
system for Barrett’s esophagus: the Prague C & M criteria. Gastroen-
terology. 2006;131:1392–1399.)
4
2
0
metaplasia:
M = 5.0 cm
Circumferential extent
of metaplasia:
C = 2.0 cm
Tr ue position of GEJ:
Origin = 0.0 cm
Abnormalities of the gastroesophageal ap valve (gastric
portion of the LES) can be visualized by retroexion of the
endoscope. Hill and colleagues graded the appearance of
the gastroesophageal valve from I to IV according to the
degree of unfolding or deterioration of the normal valve
87
architecture (Fig. 15-10).
e appearance of the valve correlates with the presence of increased esophageal acid exposure, occurring predominantly in patients with grades III
and IV valves. Grade IV valve is compatible with a hiatal
hernia. A hiatal hernia is endoscopically conrmed by the
nding of a pouch lined with gastric rugal folds residing
2 cm or more proximal to the margins of the diaphragmatic crura. e presence of hiatal hernia is often associated with an increased esophageal exposure to gastric juice.
When a paraesophageal hernia (PEH) is found, a gastric
ulcer (Cameron ulcer) or gastritis within the hernia should
be excluded. Patients who present with anemia and a PEH
with Cameron’s ulcers should also have colonoscopy to rule
out blood loss from a colon cancer.
Measurement of Gastroesophageal
Reux
AMBULATORY pH MONITORING
Fuchs and colleagues demonstrated that 24-hour esophageal
pH monitoring had a very high sensitivity and specicity
(96%), as well as positive and negative predictive values
Chapter 15 Gastroesophageal Reux Disease and Hiatal Hernia (Including Paraesophageal) 329
GRADE I GRADE II
A B
GRADE IVGRADE III
C D
FIGURE 15-10 Hill classication. A. Grade I ap valve appearance. Note the ridge of tissue that is closely approximated to the shaft of the
retroexed endoscope. It extends 3–4 cm along the lesser curve. B. Grade II ap valve appearance. e ridge is slightly less well dened than in
grade I and it opens rarely with respiration and closes promptly. C. Grade III ap valve appearance. e ridge is barely present, and there is often
failure to close around the endoscope. It is nearly always accompanied by a hiatal hernia. D. Grade IV ap valve appearance. ere is no muscular ridge at all. e gastroesophageal valve stays open all the time, and squamous epithelium can often be seen from the retroexed position. A
hiatal hernia is always present. (Reproduced from Hill LD, Kozarek RA, Kraemer SJ, et al. e gastroesophageal ap valve. In vitro and in vivo
observations. Gastrointest Endosc. 1996;44:541.)
(96%), with an overall accuracy of 96%.19 Since this study
was reported, 24-hour esophageal pH monitoring has been
a gold standard for the diagnosis of GERD. It is particularly
important that preoperative pH testing be performed o
medication in patients being considered for antireux surgery
to evaluate the symptom correlation with reux events and
the severity of the disease. Antisecretory medications should
be discontinued 10–14 days prior to the study. An abnormal
pH score with good symptom correlation has been shown
to be the most important predictor of a successful outcome
following antireux surgery.
Despite being the most reliable technique for quantifying acid exposure in the distal esophagus, catheter-based
24-hour ambulatory pH monitoring has signicant methodological limitations. e nasally passed pH electrode is
uncomfortable and can lead patients to minimize or avoid
reux-provoking stimuli such as diet and physical activity,
thus potentially resulting in a false-negative result. In addition, esophageal shortening during deglutition results in
movement of the pH sensor closer to LES, thus potentially
6,88
leading to a false-positive result.
In addition, patients
with atrophic gastritis may be achlorhydric and have nonacid reux that is not detected with pH testing. e recent
development of a wireless pH capsule that can be implanted
in the esophagus and transmit pH data to an external
receiver has signicantly changed patient tolerability and
capability of performing extended recording periods of 2–4
8,89
days.
In addition, extended pH monitoring using wireless technology may improve the detection of reux and
increase the sensitivity of pH testing. Several studies have
demonstrated that increasing the recording period from 24
to 48 hours results in an improvement in sensitivity of pH
7,8
monitoring by 10–26%.
Several studies have also consis-
tently demonstrated higher acid exposure values on day 2
330 Part III Esophagus
compared to day 1 with the wireless pH capsule. 10 e pH
probe should be correctly placed 5 cm (the capsule is placed
6 cm proximal to the LES or endoscopically measured anatomic GEJ) above the proximal border of the LES. is
location minimizes potential noise from proximal stomach
acid exposure, at the expense of decreased sensitivity.
Results of 24-hour pH monitoring are expressed in the
12
form of a DeMeester score.
Six variables are measured and
factored in to this composite score:
•
•
with a pH less than 4
•
with a pH less than 4
•
with a pH less than 4
•
•
e rst four of these factors evaluate the frequency and
severity of re ux, and the last two assess the ability of the esophagus to clear acid. Normal values for these six components were
determined from 50 asymptomatic control subjects. e mean
values for esophageal acid exposure and 95th percentile results
12
are shown in Table 15-5 .
COMBINED MULTICHANNEL INTRALUMINAL
IMPEDANCE-pH MONITORING
Combined multichannel intraluminal impedance-pH
(MII-pH) detects the intraesophageal bolus movement on
the basis of a change in the resistance to electric current
across adjacent electrode pairs positioned in a serial manner along a catheter. Multiple electrodes positioned along
the axial length of the impedance catheter can determine
the proximal extent of a re ux event. Air has a high impedance, whereas liquid has a greater conductivity and a lower
impedance ( Fig. 15-11 ). Based on this, it is capable of differentiating antegrade (swallow) from retrograde (re ux)
TABLE 15-5: NORMAL VALUES FOR
ESOPHAGEAL EXPOSURE TO pH <4 (N = 50)
Component Mean SD 95%
Total time 1.51 1.36 4.45
Upright time 2.34 2.34 8.42
Supine time 0.63 1.0 3.45
No. of episodes 19.00 12.76 46.90
No. >5 min
Longest episode 6.74 7.85 19.80
SD, standard deviation.
Reproduced, with permission, from DeMeester TR. Gastroesophageal re ux
disease. In: Moody FG, Carey LC, et al, Scott Jone R, eds. Surgical Treatment of
Digestive Disease . Chicago, IL: Year Book Medical; 1990:81.
0.84 1.18 3.45
bolus transit regardless of the composition of re ux (ie,
liquid, gas, mixed) ( Fig. 15-12 ). A pH monitor incorporated into the impedance catheter allows for simultaneous
detection of both acid and nonacid contents. e con guration of impedance catheters can be modi ed depending
on what type of re ux is targeted (ie, laryngopharyngeal
re ux). MII-pH is a transnasal catheter-based system and
the recording has been limited to 24 hours. As a result of
the ability to detect, localize, and classify re ux events as
acid, weakly acid, or nonacid, MII-pH has been posited as
the future standard for re ux detection and monitoring,
especially in patients with persistent typical and/or atypi-
27,
cal GERD symptoms despite PPI therapy.
clinical utility of MII-pH is still being investigated.
33 However, the
25
ASSESSMENT OF ESOPHAGEAL
BODY AND LES FUNCTION
Esophageal Manometry
Esophageal manometry is the most accurate method to assess
the coordination and pressure of the lower esophageal sphincter (LES) and the esophageal body. Patients with GERD may
have manometric ndings of a defective LES or impaired
esophageal motility. Manometry is an important component
in the preoperative workup of patients who are candidates for
antire ux surgery. First, this form of testing excludes achalasia
that may be occasionally misdiagnosed as GERD. Second,
esophageal manometry characterizes the esophageal motility,
and this information will be used to determine the surgical
approach (Nissen or partial fundoplication). Finally, manometry enables measurement of the precise location of the LES
for accurate pH probe placement.
Esophageal manometry used to be performed using waterperfused catheters with lateral side holes attached to transducers outside the body. Usually a train of ve pressure transducers are bound together with the transducers placed at 5
cm intervals from the tip and oriented radially at 72 degrees
from each other around the circumference of the catheter.
e recent introduction and clinical application of high-resolution manometry (HRM) has made esophageal manometry
simple, fast, and accurate. e basic concept of HRM is that
by vastly increasing the number of pressure recording sensors
and decreasing the spacing between them, one can monitor
intraluminal pressure without spatial gaps between recording sites or temporal gaps between sampling times. Consequently, the morphology of the gastroesophageal junction
pressure and esophageal peristalsis can be dynamically monitored in real time and a consistent fashion with normal respiration and with minimal movement-related artifact. HRM
is performed using a solid-state manometric assembly with
36 circumferential sensors spaced at 1 cm intervals (O.D.
4.2 mm) (Sierra Scienti c Instruments Inc., Los Angeles,
CA). is catheter allows each of the 36 pressure sensing elements to detect pressure over a length of 2.5 mm in each of
Chapter 15 Gastroesophageal Reux Disease and Hiatal Hernia (Including Paraesophageal) 331
Impedance
17 cm
15 cm
9 cm
7 cm
5 cm
3 cm
LOS
pH
Baseline
Impedance (Ohms)
B
Entry
Air
Bolus
Nadir
Contraction
Exit
Time
A
FIGURE 15-11 Combined multichannel intraluminal impedance-pH (MII-pH). A. Conguration of an impedance catheter. B. Structure of a
typical appearance of a bolus. As a food bolus propagates down the esophagus, it pushes a pocket of air distally (small upward spike in impedance);
as the bolus bridges the electrode pair, conductivity is increased and impedance drops; when the bolus passes the electrode pair, the resting
impedance is restored.
FIGURE 15-12 Typical tracing of a retrograde bolus movement (reux) on multichannel intraluminal impedance (MII-pH). As the bolus
bridges the electrode ring sets, the impedance decreases. e proximal extent of the bolus is traced as it crosses proximally located electrode pairs
within the esophagus.