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292 Part III Esophagus
FIGURE 14-1 Type I hiatal hernia or sliding hiatal hernia.
(Oelschlager B, Eubanks T, Pellegrini C. Sabiston Textbook of Surgery,
18th ed, Chapter 42.)
Clinical Presentation
Presentation of patients with PEH can vary widely from an
incidental nding to an emergent presentation involving
strangulation. Symptoms are often nonspecic and can
include nausea, dysphagia, dyspnea, heartburn, regurgitation,
bloating, chest pain, abdominal pain, early satiety, and aspiration leading to pneumonia. Severe pain is an ominous sign
and usually indicates volvulus or incarceration evolving to
strangulation. Symptoms can also be vague and intermittent
with patients experiencing relief of their symptoms with shifting of their hernia contents or with relief of visceral torsion.
Iron deciency anemia resulting from gastrointestinal
(GI) bleeding due to mucosal ischemia is a common presenting nding in patients with PEH, aecting over one-third
of patients with this condition.
1
is results from mucosal
FIGURE 14-2 Type II hiatal hernia. (Oelschlager B, Eubanks T,
Pellegrini C. Sabiston Textbook of Surgery, 18th ed, Chapter 42.)
FIGURE 14-3 Type III hiatal hernia. (Oelschlager B, Eubanks T,
Pellegrini C. Sabiston Textbook of Surgery, 18th ed, Chapter 42.)
Chapter 14 Benign Esophageal Disorders 293
irritation and ischemia occurring at the neck of the hernia
sac where the crura are extrinsically compressing and rubbing against the gastric fundus, resulting in the linear gastric
1–3
erosions known as Cameron’s ulcers.
It is usually not until
after exhaustive workup for other causes of anemia that the
diagnosis of PEH as the oending agent is obtained. Surgical
correction of the hernia results in resolution of the anemia.
4
While the natural history of paraesophageal hernias is not
clearly known, it is known that many of these hernias are
incidental ndings. ey are commonly discovered on chest
x-rays, CT scans, or during upper endoscopies being performed for other reasons. is is revealing as it tells us that
the true incidence remains unclear.
Diagnosis and Evaluation
e physical examination is frequently unimpressive and
nonspecic in these patients. Abdominal examination is
usually unremarkable. Chest examination with auscultation may reveal decreased breath sounds on the aected side
or the presence of bowel sounds within the chest. It is not
uncommon for patients to undergo extensive workup for
noncardiac chest or abdominal pain, ultimately arriving at
upper GI (UGI) evaluation with which the diagnosis is made.
Upper GI endoscopy and imaging studies are the mainstays
of diagnosis and evaluation.
Imaging Studies
Chest x-rays, whether obtained for entirely unrelated reasons
or not, can give the diagnosis of PEH. Common ndings on
chest lms include a retrocardiac air-uid level, resulting from
an intrathoracic stomach (Fig. 14-4). Coiling of a nasogastric
tube above the diaphragm is another classic nding.
e upper GI barium swallow/esophagogram is an essential part of the workup for these patients and often gives the
most accurate information regarding the hernia’s anatomy
and position, as well as the location of the gastroesophageal junction. It can also oer some functional information
regarding esophageal peristalsis and reux, though it is not
the best test to evaluate esophageal function (Fig. 14-5).
Computed tomography (CT) is not typically used in the
workup of PEH. Its frequent use in patient workup for other
reasons often leads to diagnosis of PEH when present. CT
is a good modality to dierentiate from other hernias of the
diaphragm such as Morgagni’s hernia or to evaluate hernia
contents in a type IV hiatal hernia.
FIGURE 14-4 Chest x-ray—retrocardiac air-uid level (arrow)
resulting from intrathoracic stomach with paraesophageal hernia.
(Used with permission from Saurabh Khandelwal, MD, University
of Washington.)
are both seen best on retroexion. Navigating the anatomy
can be a challenge as displacement and extrinsic compression
of the esophageal lumen or stomach alter anatomic landmarks. An important part of the endoscopic evaluation is to
screen for Barrett’s esophagus and malignancy. e presence
of either of these can alter therapy.
Manometry and pH Testing
Ambulatory pH testing and esophageal manometry may be
useful adjuncts in the workup of PEH. ey can be technically
Endoscopy
Flexible esophagogastroduodenoscopy (EGD) is an extremely
useful diagnostic test and one that is necessary as part of the
workup for PEH. EGD allows the operator to evaluate the
gastroesophageal junction and the size of the hernia, which
FIGURE 14-5 Upper gastrointestinal (GI) barium study. Type III
hiatal hernia demonstrated. (Used with permission from Saurabh
Khandelwal, MD, University of Washington.)
294 Part III Esophagus
hard to perform, as intubation of the LES may be impossible
to achieve due to anatomic distortion. Clarifying esophageal
function in these patients with manometry, while useful, very
rarely changes our operative plan. Only under circumstances
of complete aperistalsis of the esophagus do we deviate from
performing a routine Nissen fundoplication as part of the
PEH repair. In these circumstances, either the fundoplication
is omitted, or a partial fundoplication (Dor or Toupet) is performed. Because of the diculty in successfully performing the
test and because reux is addressed surgically in our standard
PEH repair with Nissen fundoplication, we do not mandate
24-hour pH testing. For those who perform fundoplication
selectively, it may make even more sense to pursue 24-hour
pH studies. at said, preoperative pH studies are probably a
poor predictor of GERD after repair if a fundoplication is not
done, because the hernia itself stretches the phrenoesophageal
membrane and the other natural antireux anatomy. In other
words, even if patients do not have GERD before repair, most
will develop GERD if a fundoplication is not employed. For
patients whose symptoms are primarily related to suspected
GERD, pH monitoring should be done to conrm the reason
for surgical intervention.
Indications For Treatment
8
is a reasonable strategy.
We believe that this is a reasonable
approach, especially in elderly patients with multiple comorbidities and asymptomatic hernias. We have found their data
to be consistent with our clinical experience. Young (<65
years) and t patients, even if not symptomatic, should
probably be considered candidates for repair because they
have many years to become symptomatic or develop an acute
volvulus. Obviously, patients who are symptomatic or who
have demonstrated progression of their symptoms should be
evaluated and taken for elective repair if their medical condition allows.
Therapeutic Controversies
Widely diering opinions exist regarding the aspects of surgical management for paraesophageal hernias. ey center
on the ideal approach, the use of mesh, management of the
shortened esophagus, and the use of fundoplication. As one
develops an operative strategy, it is important to keep in mind
the fundamental steps that are considered universal in PEH
repair: reduction of the stomach into the abdomen without
tension, excision of the hernia sac, reapproximation of the
crura, and anchoring of the stomach.
e indications for operating on patients with PEH continue to evolve over time. Earlier surgical tenets deemed the
diagnosis of PEH an indication for surgical correction. is
was largely in part due to retrospective observations, published by Skinner, Belsey, and Hill in the late 1960s and early
1970s and from other small case series or reports in which
a high incidence of complications and mortality associated
with observation or emergent operation was observed. Skinner followed 21 asymptomatic patients, of which 6 (29%)
developed complications of bleeding, perforation, or strangulation with observation. is, in addition to an observed
pooled mortality rate of 17% with emergent operation but a
1% mortality rate with elective repair, led to the recommendation that all patients t for surgery should undergo repair
5–7
of PEH.
We now know that these hernias are not always
symptomatic, often discovered incidentally, less likely than
previously thought to present with acute complications, and
may not necessarily require repair.
Recently, Stylopoulos and colleagues performed a
population-based study showing that mortality rates associated with observation to be lower than previously reported,
and the mortality associated with emergent operation to be
5.4% rather than 17%. eir study used a population-based
decision model to estimate the risk of watchful waiting versus repair in a cohort of 5 million patients, using available
data from the 1997 Nationwide Inpatient Sample (NIS) on
PEHs. ey estimated that the perioperative mortality rate of
those undergoing elective repair to be 1.4% and the annual
risk of complications associated with watchful waiting to
be 1%. As a result, they concluded that watchful waiting
in an asymptomatic or minimally symptomatic population
OPERATIVE APPROACH
Laparoscopic, open laparotomy, and transthoracic approaches
have been described for PEH repair. Each has advantages and
disadvantages. oracotomy oers excellent visualization and
it is easier to perform gastroplasty for esophageal lengthening
from this approach. Performing a fundoplication from the
chest, however, is dicult to accomplish. is approach confers the most morbidity, with longer hospital stays, need for
single-lung ventilation, and postoperative chest-tube drainage. Open laparotomy approach is familiar to most surgeons,
avoids a chest incision and its associated morbidity, and
may result in decreased operative time. Visualization of the
mediastinal structures and exposure of the hiatus, however,
are dicult with this approach.
e laparoscopic approach overcomes many of the
drawbacks of the two conventional open approaches. It provides
good visualization of the hiatus and mediastinal structures, and
allows for easier creation of a fundoplication. High mobilization of the esophagus into the mediastinum is possible. Avoiding the chest as an open operative eld eliminates the need for
single-lung ventilation, chest tubes, and the postoperative pain
associated with thoracotomy. Since the introduction of laparoscopic techniques, many studies have conrmed its feasibility,
9,10
safety, quicker recovery, and shorter length of stay.
While
our approach is laparoscopic, we cannot overemphasize that
these are complex operations to perform laparoscopically, even
for those with advanced laparoscopic foregut experience. ey
should be left in the hands of experienced laparoscopic foregut
surgeons. No randomized clinical trials have been performed
comparing the various approaches.
Chapter 14 Benign Esophageal Disorders 295
17
CRURAL REPAIR
As recurrence is a major outcome measure with any hernia
repair, it is important to examine the crural repair component of PEH repair. Crural repair and its longevity, as with
any hernia repair, depends on a tension-free closure. Many
strategies have been employed to overcome the tendency
toward recurrence and improve the chances of healing at the
hiatus. ese have included the use of pledgets, relaxing incisions, and various types of prosthetic mesh. Two randomized
result in erosions or strictures.
brosis at the hiatus have been reported with biologic mesh,
but not erosion. A recent review of mesh-related complications by Stadlhuber and colleagues summarizes the current
literature in this regard.
18
we feel that the true incidence is likely underreported. At this
time, we feel that biologic mesh oers the best ecacy and
safety prole of the available hiatal mesh prostheses, and do
recommend its use during PEH repair.
Problems with stenosis and
Like most surgical complications,
trials comparing hiatal closure with and without mesh were
11,12
performed by Frantzides et al and Carlson et al.
Carlson’s study randomized patients with PEH to simple suture
cruroplasty or cruroplasty with polytetrauoroethylene
(PTFE) and all patients had a Nissen fundoplication. ey
showed a reduction in hiatal hernia recurrence in patients
who received a mesh closure (18.8% recurrence with simple
cruroplasty vs 0% recurrence with PTFE-reinforced cruroplasty). Frantzides performed a study that included patients
with all types of hiatal hernia (type I–IV) in which patients
with hernia defects of greater than 8cm were randomized to
simple suture cruroplasty or cruroplasty with PTFE mesh.
At a median follow-up of 2.5 years, a 22% recurrence rate
with simple cruroplasty was observed and no recurrences
with mesh repair.
Initial enthusiasm and results, mostly from small series,
have been tempered with increasing reports of complica-
ROUTINE FUNDOPLICATION
Routine partial or total fundoplication should be performed
at the time of PEH repair for several reasons. First, there is a
signicant incidence of postoperative abnormal acid exposure
19,20
as seen on 24-hour pH testing.
In addition to the already
abnormal gastroesophageal junction anatomy associated with
PEH, further dissection at the time of surgery likely disrupts
this natural barrier even more, eliminating its contribution to
the natural antireux mechanism of the hiatus. Second, the
creation of a fundoplication acts as a gastropexy mechanism
anchoring the stomach below the diaphragm, likely reducing
recurrence rates. Total fundoplication (360 degrees) has not
been associated with increased rates of dysphagia in patients
21,22
with impaired peristalsis.
In cases of complete aperistalsis,
a partial fundoplication is a reasonable option.
tions at the hiatus because of prosthetic mesh placement,
including migration, infection, dysphagia, and erosion into
the esophagus. Polypropylene exhibits signicant shrinkage
due to hydrolysis and adhesions, and we do not recommend
Operative Technique: Laparoscopic
Paraesophageal Hernia Repair
its use at the hiatus. PTFE produces fewer adhesions, but
13
erosion into the esophagus can occur.
Erosion into the
esophagus is a serious complication that usually requires
esophagogastrectomy for treatment and is a matter of high
consequence.
Our preference has been to use a biologic mesh product
to reinforce the primary closure. Biologic meshes act as a
collagen-based absorbable bioscaold into which native tissue
ingrowth occurs. ese materials potentially address the concerns of erosion, infection, and dysphagia associated with per-
14
manent prosthetic mesh placement at the hiatus.
To test this
POSITIONING AND PORTS
e patient is positioned in the low lithotomy position, using
a beanbag and gel pad to form a padded mold for support.
e operation is performed in the steep reverse Trendelenburg’s position (Fig. 14-6).
Access and insuation are obtained per the surgeon’s preference. We gain access at the left upper quadrant, immediately
below the costal margin, using a Veress needle and an optical
bladed trocar. Our ports are placed in what we refer to as our
standard esophageal operating position (Fig. 14-7).
approach, we conducted a multicenter randomized trial in
which patients were randomized to primary repair (n=57) or
primary repair buttressed with a biologic prosthesis (n =51,
small intestinal submucosa [SIS]). e primary outcome
measure was recurrence seen on UGI. Upon completion
of our study, we observed a reduction in hernia recurrence
rate from 24% down to 9% in 95 patients at 6 months.
While our results only represent a 6-month follow-up, Jacobs
and colleagues demonstrated excellent results with SIS mesh
cruroplasty at a median follow-up of 28 months without
complications and with similarly low recurrence rates.
Desai and colleagues performed a histologic analysis at 1-year
follow-up in a canine model in which SIS mesh was used
to repair hiatal defects. ey demonstrated that good tissue
ingrowth occurred and that SIS mesh cruroplasty did not
DISSECTION
e surgeon begins by gently reducing the stomach into the
abdomen. e short gastric vessels are then divided using an
appropriate energy source. ese vessels are usually long and
15
attenuated due to the fundus’ displacement into the chest, and
they will lead to the base of the left crus. We use a left crus
approach as our group previously described.
is sharply entered using electrocautery at the base of the left
16
crus. It is important to stay in the correct plane and divide
23
the entire hernia sac. Great care must be taken to avoid injuring the crural pillars, which are usually thin and attenuated.
e dissection between the sac and the mediastinal structures
is carried up and to the right, proceeding circumferentially
e hernia sac
296 Part III Esophagus
taken higher if needed. e goal is to dissect enough so that
the gastroesophageal junction lies easily and without tension
within the abdomen. Once the sac is reduced and the esophagus mobilized, the sac is resected en bloc, beginning to the
left of the anterior vagus nerve. We feel this aides with the
creation of the fundoplication by keeping this extra tissue out
of the wrap.
CRURAL REPAIR
Posterior crural reapproximation is the next step after mobilization of the esophagus is completed. Either intracorporeal
suturing with free needles or a laparoscopic suturing device
can be used. We begin inferiorly just above the median arcuate ligament and proceed up the pillars with our sutures.
Depending on the size of the defect, three to eight no. 0 or 1
braided, nonabsorbable sutures are placed in interrupted fashion. e 52F bougie can be advanced into the stomach at this
time to gauge the cruroplasty. e tip of a blunt instrument
should pass in the space between the bougie-lled esophagus
and the reapproximated crura. On rare occasions, the nal
posterior crural sutures, if placed, can cause excessive anterior
FIGURE 14-6 Patient in low lithotomy position for optimal access
and exposure for the hiatus.
around the hiatus. e anterior vagus nerve (as it is often
displaced away from the esophagus by the sac and is easily
divided) and the esophagus must be clearly identied. e
esophagus is distorted, and identication is aided by the careful passage of a lighted bougie placed in the esophagus. e
bougie should be pulled back once the esophagus is identied,
as traction against it can lead to perforation.
If an aberrant left hepatic artery is encountered, all
attempts should be made to preserve it. e sac is then dissected o the right crus, taking care to identify and not injure
the posterior vagus nerve. Great caution must be taken to
identify and avoid injuring the left gastric artery and vein as
they may be stretched and entering the mediastinum. Once
the hernia sac is released and reduced from the mediastinum, ½-in Penrose drain is placed around the esophagus at
the gastroesophageal junction and used to provide traction.
e assistant, through the left ank port, grasps the drain to
manipulate the esophagus in order to provide exposure.
All of the hernia sac should be reduced, after which
mediastinal dissection is carried out to free up the esophagus and gain length. Dissection of the esophagus is routinely
carried up to the level of the pulmonary veins and can be
SLH
LR
Camera
FIGURE 14-7 Port placement for access to the hiatus. ARH,
assistant’s right hand; LR, liver retractor; SLH, surgeon’s left hand;
SRH, surgeon’s right hand. (Used with permission from Saurabh
Khandelwal, MD, University of Washington.)
SRH
ARH
Chapter 14 Benign Esophageal Disorders 297
FIGURE 14-8 Schematic of paraesophageal hernia (PEH) repair
with U-shaped mesh in position. (Used with permission from Saurabh
Khandelwal, MD, University of Washington.)
angulation of the esophagus. In this case, we omit them and
place anterior crural sutures using the same technique.
A biologic mesh is next used to buttress the crural repair. A
U-shaped mesh is fashioned, using six-ply mesh, and axed
to the apex of the right and left crura with suture, then
secured posteriorly with brin glue (Fig. 14-8).
FUNDOPLICATION
Fundoplication is then performed over a bougie to ensure
appropriate sizing. To ensure correct geometry and positioning of the fundoplication, we rst place a marking suture
posteriorly on the fundus 3 cm below the gastroesophageal
junction and 2 cm from the greater curve. is is brought to
the patient’s right side posteriorly through the retroesophageal
window, at which point this suture is grasped. A mirror image
is created with the anterior fundus, and they are brought
together at the 10 o’clock position at the hiatus. A “shoeshine”
maneuver is performed, bringing the posterior fundus back
through the retroesophageal space to the left side, checking to
see that an equal length of fundus is used on either side of the
greater curve, as marked by the ligated short gastric vessels.
is ensures that, when constructed, the sutures on the wrap
should be 180 degrees opposite the greater curve.
Four sutures are placed, 1 cm apart, to create a 3-cm wrap.
is is done over a 52F bougie. ree additional coronal
sutures are placed. e rst two are placed on the left and
right sides respectively, through the top of the fundoplication, taking a good bite of the esophageal muscle, and nally
through that respective right or left crus. e last suture is
placed posteriorly where the fundoplication lies naturally
against the now closed hiatus (Fig. 14-9).
FIGURE 14-9 Construction of Nissen fundoplication after
paraesophageal hernia (PEH) repair. (Oelschlager B, Eubanks T,
Pellegrini C. Sabiston Textbook of Surgery, 18th ed, Chapter 42.)
For the open technique, essentially the same steps are taken
but through a midline incision.
MOTILITY DISORDERS
Spastic Motility Disorders
Primary esophageal motility disorders (PEMDs) encompass
both spastic disorders and achalasia. Spastic disorders
include nutcracker esophagus, diuse esophageal spasm
(DES), and hypertensive lower esophageal sphincter
(HLES). ese rare disorders can present with variable or
nonspecic symptoms and can be dicult to diagnose and
treat. Symptoms frequently include chest pain, GERD,
regurgitation, and less commonly dysphagia. e clinician
must pay careful attention to presenting complaints and
beware of what symptoms typically respond to treatments
and which do not. It is important to distinguish between the
primary motility disorders just mentioned and those symptoms secondary to GERD. GERD is a signicant cause of
esophageal dysmotility and should be evaluated for its presence. Its successful treatment, medically or surgically, often
mitigates the symptoms suered by many patients. ese
patients may be initially diagnosed with esophageal motility
disorders but in actuality have a signicant reux component to their problem.
motility disorders can include diabetes mellitus, Chagas’
disease, collagen vascular diseases, and multiple sclerosis. If
such conditions exist, their severity and prognosis should
be taken into consideration when forming a diagnosis and
prior to embarking on any therapy.
24–27
Secondary causes of esophageal
298 Part III Esophagus
PATIENT PRESENTATION AND EVALUATION
Prior to investigation of the esophagus as the cause of symptoms, a cardiopulmonary evaluation should be performed to
rule out the heart or lungs as the cause. e evaluation of motility disorders should include a careful history taking. is may
help clarify the diagnosis and should allow the examiner to pick
up on any confounding psychiatric illness or disorder that may
be responsible, such as rumination syndrome. A systematic
workup should include endoscopy and UGI barium swallow to
evaluate the anatomy and rule out malignancy or other lesions
as a cause. Esophageal manometry is an essential component
of the workup, and 24-hour pH study should be performed to
evaluate for reux (Fig. 14-10).
DIFFUSE ESOPHAGEAL SPASM
Diuse esophageal spasm (DES) was rst described by
28
Osgood in 1889.
Typically, patients aected by DES will
complain of chest pain and dysphagia, and may present with
functional obstructive symptoms. Symptoms of DES can be
dicult to distinguish from GERD; both pH and manometry should be performed as part of the workup to evaluate the
patient. If abnormal reux is found on testing, the rst treatment strategy should be to control GERD with antisecretory
therapy. e dening characteristics of DES on manometry
include greater than 10% (but <100%) of wet swallows
that are followed by simultaneous esophageal contractions
29,30
of amplitude 30 mm Hg or greater (Fig. 14-11).
LES
dysfunction, manifested by improper relaxation and/or
hypertensive state, is seen in over half of patients diagnosed
31
with DES.
Intermittent peristalsis and prolonged contractions are also ndings seen on manometry. DES is a rare true
nding and is estimated to be found only in 3–5% of patients
32
evaluated for an esophageal motility disorder.
Whereas
previously there was thought to be little role for surgical treatment in DES, more recent reports of small series have shown
good results for relief of dysphagia after esophageal myotomy
in up to 80% of highly selected patients, while chest pain
24,31,33
is more dicult to cure.
A careful, thorough workup
and exclusion of GERD as a confounding factor should be
done before attempting to diagnose and surgically treat DES.
Medical management is an appropriate initial approach.
NUTCRACKER ESOPHAGUS
Nutcracker esophagus (NE) was rst described by Brand and
34
associates
later.
in 1977 and named as such by Castell several years
35
Typical presenting symptoms of patients with NE
include chest pain and less frequently dysphagia. Its dening
characteristics on manometry include hypertensive esophageal
contractions of greater than 180 mm Hg (Fig. 14-12). Patti
and colleagues performed myotomy for these patients and
observed that dysphagia was controlled in 80% of patients,
31
but that chest pain persisted in 50% of them.
Interestingly,
in the patients with recurrent pain, they developed dysphagia
postoperatively, possibly because of weakening of peristalsis
by performing the myotomy. Most patients with this manometric nding consistent with NE and presenting with chest
pain do not need an operation, and consideration for surgery
should rather be carefully given to patients with dysphagia as
the presenting symptom. e best candidates may be a small
subgroup in which manometry demonstrates a hypertensive
LES in addition to NE ndings as well as a functional obstruction on UGI. As with DES, one must evaluate for GERD
and treat if present. GERD, when present in conjunction with
hypertensive esophageal contractions, can be an inciting factor
causing further esophageal irritation in a hypersensitive esophagus. erapy aimed at correcting abnormal acid exposure and
irritation can lead to signicant improvement in symptoms.
e mainstay of treatment is medical therapy. Calcium channel blockers have shown benet in symptom improvement.
36
Tricyclic antidepressants may also provide symptom relief and
benet to patients.
HYPERTENSIVE LOWER ESOPHAGEAL SPHINCTER
Hypertensive lower esophageal sphincter (HLES) is a condition dened as having a resting LES pressure of greater than
45 mm Hg with intact, normal peristalsis (Fig. 14-13).
Incomplete relaxation of the LES may also be a feature. e
37
condition was rst described in 1960.
Patients with HLES
can be a heterogeneous group and can present with symptoms of chest pain and/or dysphagia. ey may also have
symptoms of a functional obstruction at the LES. Presentation can be with isolated symptoms or in association with
GERD. Careful history taking and a thorough workup with
manometry and pH testing are essential to clearly dene
the symptoms andthe primary problem in terms of esophageal function. erapy should be tailored to the presenting
symptoms. Medical management to reduce LES pressures
with calcium channel blockers, botulinum toxin, and phosphodiesterase inhibitors is typically the rst-line approach in
management. ese drugs can have signicant side eects
and decreasing ecacy with time. In patients with GERD
and manometric ndings of HLES, Nissen fundoplication
has shown good results in improvement of dysphagia and
38,39
chest pain.
is suggests that reux disease may be the
etiology in these patients. Patients with dysphagia or chest
pain as their predominant symptom and workup ndings of
only isolated HLES without GERD are more likely to benet from myotomy and partial fundoplication for symptom
relief, suggesting a primary sphincter dysfunction as the etiology of their symptoms. Good results have been reported by
several groups that have used myotomy and partial fundoplication to treat this subset of patients, with relief of symptoms
31,38,40
persisting as far as 3 years out.
While medical management is usually a reasonable rst-line, conservative approach
to treatment of HLES, in carefully selected and thoroughly
worked up patients surgical treatment with either Nissen fundoplication or myotomy and partial fundoplication (depending on manometric and pH test ndings) can produce good
results. As HLES is a rare disease with heterogeneous presentation, the importance of carefully and thoroughly working
Swallow
Chapter 14 Benign Esophageal Disorders 299
Swallow
0
5000
0
25
25
25
25
25
25
0
0
0
0
0
0
9:20.1
15 s
Normal peristalsis
10:
29
27
24
21
18
15
12
−3
−6
A
UES
relaxation
9
6
3
0
9:20.1
LES relaxation
15 s
Normal peristalsis
500
0
Ohms
%#
150
144
119
94
69
44
19
−10
mm Hg
0
10:20.7
B
LES relaxation
FIGURE 14-10 Normal swallow on manometry (conventional and high-resolution manometry [HRM]). LES, lower esophageal sphincter.
(Used with permission from Roger P. Tatum, MD, Director, University of Washington Esophageal Motility Laboratory.)
300 Part III Esophagus
0
5000
0
50
0
50
0
50
0
50
0
50
0
50
0
3:07.2
A
30 s
26
24
22
20
18
16
14
12
10
8
6
4
2
0
−2
−4
−6
15 s3:15.0 4:15.7
B
3000
2500
2000
1500
1000
500
0
Ohms
# %
150
130
110
90
70
50
30
10
−10
mm Hg
0
FIGURE 14-11 Diuse esophageal spasm (conventional and high-resolution manometry [HRM]). LES, lower esophageal sphincter; UES, upper
esophageal sphincter. (Used with permission from Roger P. Tatum, MD, Director, University of Washington Esophageal Motility Laboratory.)
Chapter 14 Benign Esophageal Disorders 301
100
0
100
0
100
0
100
0
100
0
100
0
Hypertensive (>180 mm Hg)
contractions
LES
Relaxation
2:26.0
15 s 3:26.8
A
29
27
24
21
18
15
12
−3
−6
B
Hypertensive (>180 mm Hg)
contractions
9
6
3
0
2:17. 6
LES
relaxation
30 s
2500
2000
1500
1000
500
0
Ohms
# %
150
130
110
90
70
50
30
10
−10
mm Hg
0
4:18.9
FIGURE 14-12 Nutcracker esophagus (conventional and high-resolution manometry [HRM]). LES, lower esophageal sphincter. (Used with
permission from Roger P. Tatum, MD, Director, University of Washington Esophageal Motility Laboratory.)