Impact of fundoplication on bolus transit across
esophagogastric junction
Peter J.
Kahrilas1,
Shezhang
Lin1,
Anita E.
Spiess1,
James G.
Brasseur2,
Raymond J.
Joehl3, and
Michael
Manka1
1 Division of Gastroenterology and Hepatology,
Department of Medicine, and 3 Department of
Surgery, Northwestern University Medical School, Chicago,
Illinois 60611-3053; and
2 Department of Mechanical Engineering,
Pennsylvania State University, University Park, Pennsylvania 16802-1413
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ABSTRACT |
This study analyzed
the effect of fundoplication on the mechanics of liquid and solid bolus
transit across the esophagogastric junction (EGJ). The squamocolumnar
junction was endoscopically clipped in seven controls, seven hiatal
hernia patients, and seven patients after laparoscopic Nissen
fundoplication. Concurrent manometry and fluoroscopy were
done during swallows of liquid barium and a 13-mm-diameter marshmallow.
The EGJ opening, pressure gradients, transit efficacy, and axial motion
were measured. The axial motion of the EGJ was reduced in the
fundoplication and hiatal hernia patients. The opening dimensions at
the squamocolumnar junction were similar among groups, but in each case
the constriction limiting flow to the stomach was at the hiatus and
this was substantially narrowed with fundoplication. As a result,
liquid intrabolus pressure was increased and marshmallow transit
frequently required multiple swallows. We conclude that fundoplication
limits the axial mobility of the EGJ and leads to a restricted hiatal
opening. These alterations decrease the efficacy of solid and liquid
transit into the stomach and are potential causes of dysphagia in this population.
hiatal hernia; lower esophageal sphincter; reflux disease; dysphagia
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INTRODUCTION |
DYSPHAGIA IS A PROMINENT side effect of fundoplication,
reported with a frequency of up to 43% (18, 19). In fact,
patients are advised to anticipate short periods of postoperative
dysphagia after laparoscopic Nissen fundoplication, with the usual
disclaimer that this will resolve over time. Whether or not that
"resolution" is actually a function of adaptation to an abnormal
condition is not clear. Attempts to minimize postoperative dysphagia
have logically focused on the impact of fundoplication on the
esophagogastric junction, in particular on variables of the surgical
technique, such as the size of the dilator used, the length of the
wrap, and the degree to which the fundus is mobilized during surgery (5, 7). As a result, the dilator diameter used intraoperatively to
gauge the tightness of the fundoplication has increased, the suggested
length of the wrap decreased, and full mobilization of the fundus is
advocated. Nevertheless, dysphagia remains a common side effect of fundoplication.
If there is a mechanical correlate of dysphagia after fundoplication,
it likely involves impaired bolus transit across the esophagogastric
junction, a region that exhibits unique attributes compared with the
adjacent tubular esophagus (12). Whereas the tubular esophagus empties
as a function of peristalsis, emptying of the phrenic ampulla,
encompassing the esophagogastric junction, is more complex. The phrenic
ampulla forms with longitudinal shortening of the esophagus during
peristalsis, which tents the gastric cardia through the hiatus (10).
Once formed, the ampulla is globular in shape and uniform hydrostatic
intrabolus pressure builds within it due to active contraction along
the ampullary wall [including the lower esophageal sphincter
(LES)]. Pulsatile flow from the ampulla into the stomach occurs
between diaphragmatic contractions (10, 19). Coincident with emptying,
the esophagus reestablishes its resting length, presumably achieved by
relaxation of the longitudinal muscle and elastic recoil of the
phrenoesophageal membrane. Clearly, the mechanics of the
esophagogastric junction may be substantially altered by
fundoplication, which is commonly performed for patients who had a
hiatal hernia before surgery. However, the effect of fundoplication on
the emptying mechanics at the esophagogastric junction has not been
described. Thus this study aimed to contrast the emptying mechanics at
the esophagogastric junction in normal volunteers, patients with a
hiatal hernia, and patients after successful fundoplication.
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METHODS |
Esophageal emptying of a solid and liquid bolus was analyzed with
combined videofluoroscopy and intraluminal manometry in groups of
normal subjects, hiatal hernia patients, and patients after
fundoplication to examine the influence of these conditions on
esophageal emptying mechanics. The study protocol was approved by the
Northwestern University Institutional Review Board, and written
informed consent was obtained from study participants.
Subject groups.
Subjects for this investigation were derived from a pool of normal
volunteers, patients with symptomatic reflux disease identified as
having a hiatal hernia, and patients who had laparoscopic Nissen fundoplication to treat chronic reflux disease. Neither the hiatal hernia patients nor patients who had undergone fundoplication had
evidence of Barrett's epithelium on the basis of prior, clinically indicated, endoscopic evaluation. Two of the hiatal hernia patients subsequently underwent fundoplication and were also studied in that
group. Of the nine volunteers and nine hiatal hernia patients evaluated, seven in each group (4 male, 3 female) satisfied our criteria for inclusion after endoscopic and fluoroscopic assessment of
the position of the squamocolumnar junction relative to the diaphragm
(see below). Of the seven fundoplication patients studied, four were
male and three were female. The mean ages of the participants were as
follows: controls, 38 ± 6 years; hiatal hernia patients, 44 ± 5 years; and fundoplication patients, 41 ± 4 years. All of the hernia
patients had reflux disease that was in endoscopic and symptomatic
remission as a result of maintenance therapy with a proton pump
inhibitor (n = 5) or an
H2 receptor antagonist
(n = 2). The fundoplication patients
were free of heartburn and not on antisecretory therapy.
Fundoplication.
All of the fundoplications were done by the same surgeon (R. J. Joehl).
The technique involved ligation of the short gastric vessels to
mobilize the gastric fundus from the lower pole of the spleen to the
left crux of the diaphragm for a distance of 10 cm measured from the
angle of His. The criterion for complete fundic mobilization was that,
when drawn posteriorly to the esophagus in preparation for plication,
the fundus of the stomach would remain in place without continued
traction. The fundoplication was then constructed with a 50 French
Maloney dilator placed in the esophagus, and the wrap was secured with
four sutures inclusive of the esophageal musculature so that the
estimated length of the wrap was 3 cm. Closure of the hiatal crura was
performed in all seven patients. All patients reported a period of
postoperative dysphagia, requiring caution during eating for a mean
period of 6 wk. At the time of the study, 6 ± 1 mo after surgery,
all patients were eating an unrestricted diet and reported only rare
instances of difficulty in swallowing solid food.
Manometric and fluoroscopic assessment of esophageal emptying.
Subjects were fasted overnight before undergoing an esophagoscopy under
sedation with intravenous midazolam and meperidine. During this
procedure, an 11-mm stainless steel clip was attached to the esophageal
mucosa at the squamocolumnar junction using an endoscopic clip-fixing
device (HX-3L, Olympus America, Lake Success, NY). These clips are
asymmetrical when imaged fluoroscopically, allowing the fixed end to be
easily distinguished from the free end. If the squamocolumnar junction
was irregular, the clip was attached at a location judged to be midway
between its proximal and distal extremes. After completion of the
clipping procedure, subjects were allowed to recover from sedation for
at least 1 h before proceeding with the manometric and fluoroscopic
studies. The esophagus was again imaged fluoroscopically 1 mo after the study, and clips that had not spontaneously dislodged were removed endoscopically in five subjects.
Before manometric study, subjects were imaged fluoroscopically in a
supine posture to ascertain their suitability for inclusion in the
normal or hiatal hernia groups. Two 10-ml dilute liquid barium swallows
(Liquid E-Z, E-Z-EM, Westbury, NY) were imaged to determine the level
of the diaphragmatic impression on the esophagus. Swallows imaged
fluoroscopically were recorded with a videotape recorder (Sony VO
9800). Subject groups were defined by the resting position of the
squamocolumnar junction clip relative to the level of the diaphragmatic
impression ascertained during esophageal emptying after a barium
swallow. To qualify as normal, the clip needed to be beneath the
diaphragmatic hiatus while our requirement for hiatal hernia was that
the squamocolumnar junction clip be at least 1 cm proximal to the
hiatus. Application of these criteria resulted in exclusion of two of
the nine normal subjects whose squamocolumnar junction was slightly
above the diaphragm and two of the nine hiatal hernia patients whose
squamocolumnar junction was <1 cm above the diaphragm.
Subjects were then studied with concurrent fluoroscopy and manometry. A
7-lumen silicone rubber manometric assembly with five side hole
recording sites situated at 1.5-cm intervals, one side hole 5 cm
proximal to this cluster, and one side hole 5 cm distal was used
(Dentsleeve, Bowden, South Australia). The manometric assembly had
radiopaque markers just distal to each side hole recording site. Each
catheter lumen was perfused by a low-compliance perfusion pump at 0.3 ml/min (Dentsleeve Mark II, 16-channel model), connected to a computer
polygraph set at a sampling frequency of 40 Hz (Neomedix Systems,
Warriewood, New South Wales, Australia), and processed utilizing
Gastromac software (Neomedix). Response characteristics of each
manometric channel exceeded 200 mmHg/s. Manometric tracings and
fluoroscopic images were synchronized using a video timer (model VC
436, Thalner Electronics Laboratories, Ann Arbor, MI) that encoded time
in hundredths of a second on each video frame and sent a 1-V 10-ms
pulse to an instrumentation channel of the polygraph at whole second
intervals. A swallow of 10 ml of barium and a swallow of a 13-mm
marshmallow along with 10 ml of dilute barium were done during
suspended end expiration.
Data analysis.
Initial analysis of the videofluoroscopic recordings was accomplished
without reference to the manometric data. Relevant videofluoroscopic sequences were digitized and analyzed with image analysis software (13). Structural movement was quantified using an image-based coordinate system referenced to a stationary point on a vertebral body
within the fluoroscopic field. Data were corrected for fluoroscopic magnification using the known 1.5-cm distance between the manometric sensors. Motion and opening diameter of the squamocolumnar junction were determined by tracking the motion of the mucosal clip.
"Vertical" motion was quantified relative to an axis drawn
through the center of the esophageal lumen with the point of hiatal
crossing designated as position
0, proximal locations recorded as
positive distances, and distal locations recorded as negative
distances. A horizontal axis was then drawn perpendicular to the
vertical axis, intersecting the esophageal wall at the attachment point
of the clip. The esophageal opening diameter was measured as the
distance between opposing esophageal walls along this horizontal axis.
The luminal diameter of the esophagus/gastric cardia as it crossed the
hiatus was also measured by this method. Videofluoroscopic data were
analyzed in conjunction with the manometric recordings to discern
intrabolus pressure (that obtained from within a bolus-filled luminal
segment), closure pressure (intraluminal pressure at the instant that
luminal closure is first achieved), and maximal contact pressure
(obtained from a closed, bolus-free segment) (4). All manometric
pressure values were referenced to atmospheric pressure.
Data values within test conditions were averaged and expressed as means ± SE, except for the occurrence of retrograde flow or impaired
transit, which was expressed as a percentage of the total number of
trials. Statistical comparisons among groups were made using the
unpaired t-test.
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RESULTS |
Axial movement and opening of squamocolumnar junction.
Esophageal emptying across the esophagogastric junction exhibited
distinct characteristics within each subject group. Figure 1 illustrates a typical example of emptying
mechanics for a normal subject, a hiatal hernia patient, and a patient
after fundoplication. In each case, the traced fluoroscopic images in
Fig. 1 illustrate the position of the squamocolumnar junction before
swallow, after swallowing but immediately before initial opening at the
squamocolumnar junction, at the time that the squamocolumnar junction
was maximally distended, and at the time of closure at the
squamocolumnar junction. It is evident from Fig. 1 that the axial
motion of the distal esophagus during emptying is greatest in the
normal subject, intermediate in the hernia patient, and least in the
fundoplication patient. It is also apparent from Fig. 1 that the
narrowest passage for entry into the stomach is at the diaphragmatic
hiatus rather than at the squamocolumnar junction and transhiatal
luminal diameter is markedly diminished with fundoplication. One
consequence of this is impaction of the swallowed marshmallow at the
superior aspect of the fundoplication, as evident in Fig. 1
(bottom
right). In all instances of failed
marshmallow transit, the site of hang up was at the superior aspect of
the fundic wrap.

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Fig. 1.
Opening and axial movement of the esophagogastric junction (EGJ) in a
representative normal volunteer, hiatal hernia patient, and
fundoplication patient. In each case, the panels depict the following:
top
left, configuration prior to swallow;
top
right, instant before opening at the
squamocolumnar junction (SCJ); bottom
left, point of maximal distension at
the SCJ; and bottom
right, time of closure at the SCJ.
Filled numbered circles depict position of the SCJ in current panel,
whereas open numbered circles reflect the SCJ position shown in
previous images. The two No.
3 circles indicate clip position and
estimated position of the SCJ on the opposing esophageal wall at time
of maximal distension. Impaired marshmallow transit in a fundoplication
patient is also shown. Note that the marshmallow impacts at superior
margin of fundoplication, as it did in all instances of impaired
transit.
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Figure 1 suggests that deglutitive axial motion at the squamocolumnar
junction is diminished in both hiatal hernia and fundoplication patients compared with normal subjects. Figure
2 summarizes group data on mobility and
opening of the squamocolumnar junction. The scheme of Fig. 2 is similar
to that of Fig. 1 in that the initial and extreme axial positions of
the squamocolumnar junction as well as its maximal opening dimension
are indicated. Evident from the summary data, opening dimensions at the
squamocolumnar junction are greatest among the hiatal hernia patients
and least among the normal subjects, whereas a comparison of normal
subjects to hiatal hernia patients to fundoplication patients shows
that deglutitive axial motion is progressively attenuated. The other
major distinguishing feature of the fundoplication patients is in the
reduced opening dimension across the diaphragmatic hiatus (Table
1). Associated with the diminished opening
dimension is impaired marshmallow transit across the esophagogastric
junction; while there were no instances of impaired transit among the
normal subjects or hiatal hernia patients, this was observed in four of
seven fundoplication patients (Table 1).

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Fig. 2.
Summary data on opening and axial movement of the SCJ among subject
groups. As in Fig. 1, only incremental movement of the SCJ before
opening and from initial to maximal opening
(top) and from maximal opening to
closure and descent after closure
(bottom) is shown. Position of the
SCJ is shown as follows. Top: , at
rest; , before luminal opening; , at maximal distension.
Bottom: , at maximal distension;
, at luminal closure; , after descent. Closure vector indicates
direction of luminal movement during closure; 0° is vertical and
90° is horizontal. Data are means ± SE for each subject group.
* P < 0.05 vs. normal.
P < 0.05 vs. hiatal
hernia.
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Table 1.
Opening duration at the SCJ, total axial movement of the SCJ, and
marshmallow transit across the EGJ in subject groups
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Mechanics of liquid transit across esophagogastric junction.
Along with the altered deglutitive mechanics of the esophagogastric
junction among subject groups, there were differences in the pressure
characteristics of esophageal emptying. Figure 3 depicts concurrent manometric and
fluoroscopic data for a normal subject. The traced
fluoroscopic images in Fig. 3 show the anatomic configuration at the
time of luminal closure at each recording site, and the manometric
tracings depict the activity at the corresponding times at each
recording site. Moving from the proximal to the distal sensor, the
pattern of emptying shifts from that characteristic of the esophagus,
with slight intrabolus pressure and relatively large amplitude contact
pressures during the peristaltic contraction, to that characteristic of
the ampulla with higher, sustained intrabolus pressure and no
subsequent peristaltic contraction (12). Thus Fig. 3 (manometric
tracings) indicates the pressures that are built up within the bolus to
overcome the frictional pressure drop associated with the narrowing of
the lumen as it traverses the hiatus.

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Fig. 3.
Fluoroscopic and manometric data on emptying across the EGJ in a
representative normal subject. Fluoroscopic tracings at
left depict anatomic configuration at
the time of luminal closure at manometric recording
sites
7, 6,
5, and
4 corresponding to
t7,
t6,
t5, and
t4, respectively.
Similarly, at right, the corresponding
timing of these images is indicated on manometric tracings by labeled
vertical lines. As such,
t7,
t6,
t5, and
t4 represent the
transition from recordings of intrabolus pressure (shaded on the
manometric tracings) to recordings within a closed lumen for manometric
recording sites
7, 6,
5, and
4, respectively (indicated by circled
areas on manometric tracings). Note transition from peristaltic pattern
of emptying in tubular esophagus (recording
site
7), characterized by high-amplitude
propagated contraction, to that of the ampulla (recording
sites
4 and
5), characterized by a sustained
low-amplitude contraction during restoration of esophageal length
(distal migration of clip at the SCJ).
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Figures 4 and
5 are analogous to Fig. 3, illustrating
examples of a hiatal hernia patient and a postfundoplication patient, respectively. In each of these cases, the pressure characteristics generated on the bolus as it traverses the hiatus are different from
those of the normal subject. In the hiatal hernia patient, the
magnitude of intrabolus pressure at the second and third manometric sites is low. On the other hand, in the fundoplication patient (Fig.
5), there was a rapid increase in intrabolus pressure at the fourth
manometric site immediately before luminal closure. However, with
fundoplication, Table 1 shows the transhiatal luminal diameter to be
significantly reduced. The other distinctive feature of fundoplication
was the sustained, repetitive esophageal contraction, as evident at the
sixth recording site shown in Fig. 5. Table 2 summarizes data on ampullary intrabolus
pressure and esophageal contractile activity among the subject groups.
The functional consequence of these altered pressure dynamics among
groups is evident in Table 2; incomplete esophageal emptying occurred
in three of seven fundoplication patients and two of seven hiatal hernia patients. Figure 6 summarizes the
data on closure pressure at each luminal location relative to the
squamocolumnar junction, indicating that these were significantly
decreased in the hiatal hernia patients and significantly increased in
the fundoplication patients. Note that the intragastric pressures among
subject groups were almost identical; 7.9 ± 0.6, 7.9 ± 0.5, and
7.2 ± 0.6 mmHg for the normal, hiatal hernia, and fundoplication
groups, respectively.

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Fig. 4.
Fluoroscopic and manometric data on emptying across the EGJ in a
representative hiatal hernia patient shown as in Fig. 3. In this
example, t5,
t4,
t3, and
t2 depict luminal
closure at manometric recording sites
5, 4,
3, and
2, respectively. Consistent with this
being a nonreducing hiatal hernia, bolus transfer across the hiatus is
incomplete. Note substantially reduced intrabolus pressures compared
with Fig. 3 (see Table 2 for summary data).
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Fig. 5.
Fluoroscopic and manometric data on emptying across the EGJ in a
representative postfundoplication patient shown as in Figs. 3 and 4. In
this example, t6,
t5,
t4, and
t3 depict luminal
closure at manometric recording sites
6, 5,
4, and
3, respectively.
Site
1 is 5 cm distal to
site
2, beneath the field of view. Note
substantially increased intrabolus pressure at
sites
3 and
4 compared with Fig. 3 (see Table 2
for summary data) and narrowed, elongated outflow tract associated with
fundoplication. Also note sustained, repetitive esophageal contraction
at site
6 that persists until complete
emptying is achieved.
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Fig. 6.
Luminal closure pressures in region of the EGJ among subject groups.
Squares, normal subjects; triangles, postfundoplication patients;
circles, hiatal hernia patients. Open symbols indicate position distal
to the SCJ. Position
0 is the center of the hiatus, while
negative axial positions extend into the esophagus and positive values
into the stomach. Bar on each tracing indicates position of the SCJ at
time of luminal closing. * P < 0.05 vs. normal subjects.
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DISCUSSION |
The esophagogastric junction is anatomically specialized to permit
seemingly contradictory actions. During swallow-induced relaxation, it
facilitates esophageal emptying while simultaneously preventing the
reflux of gastric contents that is favored by the positive
abdomen-to-thorax pressure gradient. At rest, it must episodically
permit belching or vomiting but prevent frequent gastric reflux. This
physiological balance is accomplished by the interplay of several
anatomic and physiological variables, including the position of the LES
relative to the diaphragm (22), the pattern of crural contraction
during LES relaxation (17), and the repositioning of the LES relative
to the diaphragm by longitudinal muscle contraction of the esophagus
(10). Two circumstances during which esophagogastric junction anatomy
is altered are the hiatal hernia and fundoplication. Previous studies
(9, 15, 22) have shown that one consequence of a hiatal hernia is
compromise of retrograde competence during swallow-induced LES
relaxation. Fundoplication is performed to correct the retrograde
incompetence of the esophagogastric junction both at rest and during
swallow. However, improved retrograde competence may come at the
expense of compromising antegrade flow. The present study suggests that fundoplication significantly alters the axial mobility of the esophagogastric junction and narrows the hiatal canal; each of these
has potential negative consequences on esophageal emptying.
Esophageal peristalsis entails both a lumen-obliterating contraction
and shortening. In the tubular esophagus, shortening results from
longitudinal muscle contraction (23, 24), and the magnitude of axial
propulsive force as measured with a balloon tethered to a
tension-sensing transducer is proportional to the magnitude of
shortening in the area of the balloon (21). This mechanism of
generating axial propulsive force is accentuated in the upper
esophageal sphincter, a region characterized by profound clearing
ability (20). Axial motion accompanies peristalsis at the
esophagogastric junction by a somewhat different mechanism; ascent is
attributable to longitudinal muscle contraction but descent depends on
relaxation of the longitudinal muscle and the elastic recoil of the
phrenoesophageal attachments. Viewed as such, the phrenic ampulla is a
small, reducing hiatal hernia (1, 8). With progressive loosening of the
phrenoesophageal ligament, the phrenic ampulla first enlarges to a
reducing hiatal hernia and then evolves into a persistent, nonreducing
hiatal hernia (6, 10, 25). Consistent with this concept of the hiatal hernia, axial motion at the esophagogastric junction during peristalsis is quantitatively reduced with a hiatal hernia (10). Findings from the
present study show an even greater decrement in axial motion after
fundoplication. Figures 2 and 6 show that the most profound decrease in
axial motion observed in the fundoplication group was in the descent
phase of emptying. During this phase, the lumen is closed by circular
muscle contraction, while esophageal length is reestablished.
Conceptually, this is analogous to the grabbing effect observed within
the upper esophageal sphincter during which propulsive force is maximal
(20). The impaired marshmallow transit observed in the fundoplication
patients suggests that decreased axial motion of the esophagogastric
junction is functionally significant. This hypothesis is also
consistent with the clinical observation that postfundoplication
dysphagia correlates more closely with the degree of intraoperative
fundic mobilization than with the completeness of the wrap itself (7).
Ampullary emptying of liquids and semisolids is altered by both
fundoplication and a hiatal hernia. Rather than by peristalsis, the
ampulla normally empties during expiration by a combination of elevated
sustained circular muscle tension and relengthening of the esophagus
(10, 12). The elevated wall tone is necessary to create a sufficient
back pressure to overcome both the elevated pressure within the stomach
relative to the esophagus and the frictional pressure drop associated
with a narrowed hiatus. The generation of intrabolus pressure within
the ampulla, the resistance to flow across the narrowed hiatal segment
separating the ampulla from the stomach, and the rate of flow across
the esophagogastric junction are mechanically interrelated by a form of
Newton's law of motion applied to flow (assuming that frictional and
pressure forces dominate over inertial and gravitational forces):
P = CV(Q/D4)
L
(4, 11). In this formula,
P is the pressure drop from the esophagus
to stomach over a luminal segment of axial extent
L, Q is the volumetric rate of flow
through the segment, D is the average
diameter of the segment, V is the
bolus fluid viscosity, and C is a
constant that depends on the cross-sectional geometry of the segment.
Note that there must always be a drop in pressure in the direction of
flow when friction dominates and that the required ampullary pressure
that must be generated is proportional to
1/D to the fourth power. Thus, given
that gastric pressure was nearly identical among subject groups (Fig.
6), small decreases in the hiatal diameter create large differences in
the pressure drop across the hiatus even if the physiological system
responds to increased resistance by decreasing the rate of flow and
extending the time for esophageal emptying. Thus the 12.5% increase in
hiatal diameter in the hiatal hernia group and the 50% reduction in
the fundoplication group (Table 1) are associated with respective reduction and increase in the intrabolus pressure integral of these
groups (Table 2). Increased intrabolus pressure proximal to
fundoplication of similar magnitude has recently been reported by
Mathew et al. (14).
A change in intrabolus pressure within the ampulla implies also a
change in "clamping" pressure required to maintain luminal closure at the tail of the ampulla (for example, recording
site 6 at
time
6 in Fig. 5). Figure 6 illustrates the
differences among groups in the pressure required to maintain ampullary
closure during emptying. Closure pressures are greatly increased in the fundoplication group and reduced (with a more proximal peak) in the
hiatal hernia group. Physiologically, increased ampullary pressure
implies increased active tension within the circular muscle of the
esophageal wall surrounding the ampulla. This statement is based on the
application of "Laplace's law"
(T = 1/2P × D) where T is tensile force per axial length of
circular muscle, P is the intrabolus pressure relative to thoracic
pressure, and D is the luminal
diameter. If the muscle of the distal esophagus is incapable of
providing the required increment in tone, the rate of flow through the
esophagogastric junction must be reduced or a failure of emptying will
occur, evidenced by retrograde flow of the bolus (Table 2). A similar
effect is observed in an esophagus obstructed by a diameter-limiting
ligature (16); the esophagus proximal to the partial obstruction
exhibits repetitive sustained contractions as evident by the tracing at
the sixth recording site in Fig. 5 and by the esophageal contraction
integral values in Table 2. This pattern of repetitive
contractions is not normally seen at the esophagogastric junction even
in the case of outflow obstruction by a Müller maneuver, because
the esophageal segment normally generating the intrabolus pressure (the
phrenic ampulla) exhibits a sustained tonic contraction rather than a
propagated peristaltic one (2, 3, 12). Thus the occurrence of these
spasmlike esophageal contractions is another consequence of decreased
mobility of the esophagogastric junction after fundoplication.
In conclusion, functional alterations of the esophagogastric junction
are evident with both a hiatal hernia and fundoplication. With a hiatal
hernia, there is a major defect in retrograde competence during
peristalsis (15, 22). Findings from the present study suggest that
fundoplication impairs antegrade transfer of both solids and liquids at
least in part because of decreased mobility of the esophagogastric
junction during peristalsis and narrowing of the transhiatal passage.
Although the subjects in this investigation did not report clinically
significant dysphagia, they exhibited objective evidence of impaired
bolus transfer that was attributable to the altered mechanics of the
esophagogastric junction consequent from fundoplication.
Further work will be necessary to determine the relationship
between these observations and clinically significant postfundoplication dysphagia.
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ACKNOWLEDGEMENTS |
This study was supported by National Institutes of Health Grant
RO1-DC-00646 (P. J. Kahrilas).
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FOOTNOTES |
The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement"
in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Address for reprint requests: P. J. Kahrilas, Division of
Gastroenterology and Hepatology, Department of Medicine, Northwestern
University Medical School, Passavant Pavilion, Suite 746, 303 East
Superior St., Chicago, IL 60611-3053.
Received 2 June 1998; accepted in final form 1 September 1998.
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Am J Physiol Gastroint Liver Physiol 275(6):G1386-G1393
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