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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1033_Библиотеки_им_академика_М_И_Перельмана
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J. F. Preston and N. J. Soper
Surgical Fundoplication
Persistent dysphagia following surgical fundoplication is reported
in 5–12% of patients [6–9]. Although persistent dysphagia may be
seen in fewer patients following partial compared to complete
fundoplication, the etiology and evaluation of persistent dysphagia in partial fundoplication is similar to complete fundoplication
[10–12]. Therefore, for the purpose of this chapter, partial and
complete fundoplication will not be differentiated except in
reporting normal post-fundoplication manometry ndings.
The etiology for persistent dysphagia can be grouped into three
main categories such as problems with the hiatal closure, which
includes both intrathoracic migration of the wrap and crural stenosis, complications of the wrap itself, including a tight, twisted
or slipped wrap, and motility disorders [7, 8, 13, 14]. The primary
diagnostic studies which help to identify the underlying etiology
include barium esophagography, endoscopy and, in some cases,
esophageal manometry [7, 13].
Barium Esophagography
A barium esophagram provides essential information in evaluating patients with persistent dysphagia as it provides the best
global assessment of anatomic problems and physiologic abnormalities contributing to dysphagia. This is because with appropriate positioning and swallowing procedures, information can be
obtained regarding overall patterns of esophageal motility and
emptying. Initially the patient should be positioned upright and
asked to ingest a small amount of low-density barium. Normal
post-fundoplication images will reveal narrowing of the distal
esophagus with a gentle curve as contrast passes through the fundoplication. There may also be a minor delay of contrast passage
through the wrap [15]. If there is a signicant delay in contrast
passing through the wrap, a timed swallow study should be performed with interval images at 2 and 5min. This will identify
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Fig. 36.1 Tight fundoplication
patients who have crural stenosis, a tight wrap or a motility
disorder such as achalasia early in the examination (Fig.36.1). In
patients with a crural stenosis or a tight wrap, there will be smooth
narrowing of the distal esophagus proximal to the wrap with dilatation of the proximal esophagus. If a timed study is not needed,
the study should continue with an air-contrast phase to help dene
the anatomy of the fundoplication. The patient should be moved
through several positions including upright, supine, left decubitus
and right anterior oblique. Several spot lms should be taken during this process. In the right anterior oblique position, the patient
should be asked to ingest additional contrast with continuous uo-
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Fig. 36.2 Intrathoracic migration of fundoplication with crural stenosis
J. F. Preston and N. J. Soper
roscopy. These maneuvers should clearly dene the location and
anatomy of the gastroesophageal junction, the level of the
diaphragm and the position and morphology of the wrap.
Intrathoracic migration of the wrap (Fig. 36.2), crural stenosis
(Fig.36.2), slippage of the proximal stomach through the wrap
(Fig.36.3) and twisting or loosening of the wrap should be identiable (Fig.36.3). Motility can be assessed using the standard
ve swallows. If motility is intact but there is an issue with a tight
fundoplication, peristalsis will be normal to the level of the epiphrenic ampulla which may balloon out, indicating a higher pressure gradient across the wrap than in the peristaltic wave. The
rapid drinking phase is also important in determining the location
of the wrap, integrity and length of the wrap, the lumen of the
wrap, and intrathoracic migration of the wrap [15, 16].
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Fig. 36.3 Intrathoracic migration of the wrap with slippage onto the stomach and loosening of the wrap
Endoscopy
Endoscopy is an important diagnostic tool in evaluating patients
with post-fundoplication dysphagia as it is particularly sensitive
in identifying structural abnormalities of the wrap itself. Key
endoscopic features that can be seen in patients with dysphagia
include a slipped, twisted, disrupted or tight wrap, intrathoracic
migration of the wrap and/or esophageal pathology such as
esophagitis. In patients with a slipped wrap, the squamocolumnar
junction will be located more than 1cm proximal to the proximal
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Fig. 36.4 Squamocolumnar junction noted proximal to wrap
J. F. Preston and N. J. Soper
margin of the wrap (Fig. 36.4). A disrupted wrap will appear
loose or twisted on retroexion (Fig. 36.5). A tight wrap may
cause resistance to endoscopic passage into the stomach, although
esophagography has been shown to be more sensitive at detecting a tight fundoplication than endoscopy. With intrathoracic
migration of the wrap, the fundoplication may appear intact, but
the hiatal pinch will be noted distal to the fundoplication
(Fig. 36.6). Lastly, esophageal mucosal abnormalities, such as
esophagitis from recurrent reux or eosinophilic esophagitis, can
also be detected endoscopically. Eosinophilic esophagitis is considered if classic concentric rings are present, as well as possible
exudates, plaques or furrows. This diagnosis is conrmed on
biopsies that demonstrate more than 15 eosinophils per high
power eld [7, 17].
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Fig. 36.5 Loosened fundoplication
Esophageal Manometry
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High-resolution esophageal manometry can be helpful in patients
with signicant dysphagia who appear to have normal postfundoplication anatomy on esophagography and endoscopy. In
order to interpret manometry ndings correctly in symptomatic
patients, however, it is important to understand the normal manometric values following fundoplication in asymptomatic patients.
There are also some differences between postoperative manometry following complete and partial fundoplication. In the following sections, the normal post-fundoplication ndings, as described
in the Chicago Classication System, will be outlined rst, followed by results in patients with dysphagia.
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Fig. 36.6 Intrathoracic migration of fundoplication
J. F. Preston and N. J. Soper
Esophagogastric Junction Parameters
For asymptomatic patients, the mean intra-abdominal esophagogastric junction (EGJ) length is similar between Nissen (2.7cm ±
1.1 cm) and Toupet fundoplication (2.7cm ± 0.8 cm). The mean
Integrated Relaxation Pressure (IRP) is higher for Nissen (13 ±
5.1 mmHg) than for Toupet (7.4 ± 2.9 mmHg) but both fall within
the normal range (<14.7 mmHg). The same is true for the EGJ
resting pressure for Nissen and Toupet (19 ± 8.3 mmHg and 12.7
± 5.7 mmHg, respectively, p < 0.01) with the normal range being
5–31.6 mmHg [18].
For patients with dysphagia, the Lower Esophageal Sphincter
(LES) resting pressure is commonly within the normal range. The
mean IRP with wet swallows will be abnormally elevated in
15–34% of patients indicating EGJ outow obstruction [19–21].
With the addition of a solid meal, the percentage of patients with
an abnormal IRP will increase to 40.7% [19]. When directly comparing IRP in patients with dysphagia to asymptomatic patients,
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the mean IRP is higher in patients with dysphagia, even though
for a majority of patients, the IRP value will still be within normal
range [22, 23]. Achalasia is a rare nding on post-fundoplication
manometry [20, 21].
The average maximal intrabolus pressure during the swallow
window in asymptomatic patients is similar between Toupet and
Nissen (13.7 ± 3.4 mmHg and 15.2 ± 3.6 mmHg, respectively),
with slightly higher upper limits of normal for both procedures
compared to the Chicago Classication (<15 mmHg) [18]. This is
true for patients with dysphagia as well [19]. When postfundoplication patients with and without dysphagia are directly
compared, there does not appear to be a signicant difference in
intrabolus pressure between these groups, with both being elevated [22, 24].
The bolus transit time after fundoplication is signicantly longer with liquids (6.8 ± 0.9 s compared to 9.8 ± 1 s, p < 0.01) and
solids (2.8 ± 0.5 s compared 5.8 ± 0.8 s, p < 0.01) for all patients
post-fundoplication indicating a decreased EGJ transit efcacy.
This is likely a result of decreased EGJ compliance postfundoplication limiting EGJ opening. There is a signicant positive correlation with increasing bolus transit times and symptoms
of dysphagia [24].
Esophageal Body Contraction Parameters/Peristalsis
In asymptomatic patients, the distal contractile integral (DCI) is
signicantly higher for Nissen than Toupet (2037 ± 1154 mmHg
vs 845 ± 538 mmHg, respectively, p < 0.01); however, the upper
limits of normal for both fall within the normal range (448–4721
mmHg) [18]. When comparing patients post-fundoplication with
and without dysphagia, there does not appear to be a signicant
difference in DCI [22, 23].
The contraction amplitude in the proximal, middle and distal
esophagus has been shown to be signicantly higher after Nissen
(63.9 ± 29.5 mmHg, 91.2 ± 42.3 mmHg, and 111.9 ± 41.6 mmHg,
respectively) compared to Toupet (42.4 ± 23.3 mmHg, 62 ± 31.5
mmHg, and 64.5 ± 27 mmHg, respectively) (p < 0.05 for proximal
and middle, p < 0.01 for distal) with the upper limits for Nissen
being higher than the 95th percentile in Chicago Classication
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(102.1, 146.4, and 146.4, respectively). However, there does not
appear to be a signicant difference in contraction amplitude preand post-fundoplication specically in patients with dysphagia
[25, 26]. The mean contractile velocity and mean distal contraction latency are similar between both Nissen and Toupet and fall
within the normal range of the Chicago Classication [18]. When
patients post-fundoplication with and without dysphagia are compared, the distal contraction latency and contractile velocity are
not statistically different [22, 25].
There does not appear to be a signicant difference in ineffective peristalsis patterns in post-fundoplication patients with and
without dysphagia. There is a statistically signicant increase in
percentage of patients with incomplete bolus clearance with dysphagia compared to patients without dysphagia (61% vs 32%,
respectively, P = 0.01) [27].
J. F. Preston and N. J. Soper
Manometry Summary
An increased mean IRP in the setting of dysphagia likely indicates an issue with the wrap. Increased bolus transit time and/or
incomplete bolus clearance may indicate either an issue with the
wrap or with crural stenosis. LES resting pressure, intrabolus
pressure, DCI, contraction amplitude and peristaltic patterns do
not appear to be signicantly different between patients with and
without dysphagia, making these parameters less useful in identifying causes for dysphagia.
Functional Luminal Imaging Probe (FLIP)
The functional luminal imaging probe is a balloon-based catheter
that uses impedance planimetry to measure diameter, crosssectional area and distensibility of the EGJ in response to volumecontrolled distension. Over the past few years, this technology has
been used to evaluate and better understand EGJ distensibility following fundoplication. When compared to controls, patients postfundoplication exhibit reduced EGJ distensibility and reduced
EGJ compliance during deglutitive relaxation and a longer segment of reduced distensibility [28]. The feasibility of utilizing this
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technology intraoperatively to aid in decision-making and to
understand postoperative outcomes is still being explored, but
recent studies have shown this to be a promising technology. Su
etal. published a series of 226 patients in which FLIP was utilized
intraoperatively [29]. During the nal year of that series, the number of procedures in which management was changed based on
FLIP measurements was recorded. During that year, management
was changed based on high or low intraoperative FLIP distensibility indices (DI) in 12 of 52 patients. The changes recorded
included additional crural sutures (high DI after closure) and
change in type of fundoplication based on high (changed to
Nissen) or low DI (changed to Toupet) [29]. In a subsequent follow- up series, that group demonstrated patients with a nal intraoperative DI < 2 mm2/mmHg experienced signicantly more
dysphagia at 1 year compared to those patients with a DI ≥ 2mm2/
mmHg. This difference became even larger at 2 years [30].
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Magnetic Sphincter Augmentation (MSA)
Persistent moderate to severe dysphagia following MSA ranges
from 1–15% in the literature and is the most common indication
for device removal [31–34]. The etiologies for persistent dysphagia include recurrent hiatal hernia, migration of the device, device
erosion, outow resistance from either crural stenosis or an undersized device, and inadequate intake of bulky food allowing the
device to be encapsulated by scar tissue in the ‘closed’ position.
Other patients experience dysphagia of unknown etiology, dened
as patients with normal testing but persistent symptoms [31, 33–
37]. With a recurrent hiatal hernia, migration of the device, and
device erosion, there will often be a symptom-free interval prior
to representation with dysphagia. The primary investigations to
identify the underlying etiology include barium esophagography
and endoscopy [31, 33, 34, 36–39]. Esophageal manometry has
not been shown to be different in patients with dysphagia compared to patients without dysphagia. For thoroughness of this
chapter, the expected manometry ndings following MSA will be
described.
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