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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_639_Библиотеки_им_академика_М_И_Перельмана.pdf
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LS
Normal Peristalsis
3:21.1
A
Normal peristalsis
15 s
Hypertensive, nonrelaxing LES
15 s
1000
500
0
Ohms
# %
150
119
94
69
44
19
−10
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0
4:17.7
B
Hypertensive, nonrelaxing LES
FIGURE 14-13 Hypertensive lower esophageal sphincter (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.)
302
Chapter 14 Benign Esophageal Disorders 303
up aected patients before embarking on therapy cannot be
overemphasized.
Summary
Spastic PEMDs (NE, HLES, DES) represent a diagnostic
and therapeutic challenge to the clinician. Careful attention
to presenting symptoms and thorough workup of esophageal function are of utmost importance for both diagnosis
and discussion with patients regarding treatment options.
Overlap with these disorders and GERD is frequent, and
GERD can signicantly contribute to and exacerbate presenting symptoms. Medical and surgical therapies have been
tried in the past, most of which share the goal of relieving
functional obstruction at the GEJ to allow for improved
esophageal clearance. In most cases, a less invasive therapeutic approach with smooth muscle relaxing agents is a
prudent rst line of therapy. Surgery may be oered to carefully selected patients in whom an operation can address a
discrete etiology such as abnormal GERD or isolated LES
dysfunction.
Achalasia
often worsen after lying supine, with regurgitation occurring
even the next day of the previous day’s meal. Cold liquids
frequently exacerbate symptoms, with inability to ingest cold
water being a common complaint. Patients may give a history of various maneuvers they employ in attempts to allow
passage of food through their nonrelaxing LES. ese include
raising their arms over their head, swallowing liquids to try
to “wash down” food, or remaining upright for extended
periods of time. It is only after overcoming the LES pressure with a column of food and liquid that exerts a greater
hydrostatic pressure that the patient is able to swallow. Prior
to severe progression of their disease, these maneuvers may
work for them. As the disease progresses and the esophagus
dilates, in eect acting like a stomach reservoir, one nds that
regurgitation of the prior day’s food contents becomes more
common. Symptoms such as these can lead to avoidance of
social situations by patients in which they fear regurgitating
food in front of others. In addition, frequent regurgitation
and aspiration can lead to pulmonary complications. Weight
loss can occur with achalasia and tends to correlate with disease severity. However, in older patients (>60 years), recent
onset of symptoms (<6months) and signicant weight loss
(>10–20 lb) should stimulate concern for neoplastic causes
otherwise known as pseudoachalasia. In such cases, patients
should be worked up with a CT of the chest and abdomen
and/or endoscopic ultrasound before therapy.
Idiopathic achalasia is a primary motor disorder aecting the
esophagus. Achalasia, which is typied by complete aperistalsis of the esophagus, is the most frequently encountered
motility disorder seen by surgeons. It is a rare condition,
with an incidence of 1–3 per 100,000 population in the
41
Western world.
It is, however, of all the previously mentioned motility disorders, the most common PEMD. e
histopathologic hallmark of the disease remains near complete or total loss of the myenteric plexus ganglion cells as
a result of injury and brosis of these cells and myenteric
nerves. Recent inquiries into the cause suggest an autoimmune disorder, as evidenced by CD3/CD8 lymphocyte
markers seen on immunohistochemical analysis of the
42–44
inammatory inltrate.
e inciting event or trigger
may relate to cytotoxic T-cell activation by latent herpes
45,46
simplex virus 1(HSV-1) antigen exposure.
In addition,
nitric oxide (NO) synthesis, a mediator of LES relaxation, is
often impaired in the face of preserved cholinergic neuronal
47–49
function.
ese two insults result in loss of peristalsis and
impaired relaxation of the LES, which in turn lead to the
pathophysiologic ndings of impaired esophageal emptying,
aperistalsis, and a nonrelaxing LES.
PATIENT PRESENTATION
Achalasia can occur in patients of all ages but typically
presents in patients in the second to fth decades of life. It
does not show a predilection toward either sex. Typical symptoms include dysphagia, regurgitation of indigested food,
and complaints of food “sticking” in the chest. Symptoms
EVALUATION
Patients should be worked up in a systematic, methodical
fashion. e workup has several components. An upper GI
esophagram should rst be performed to assess the anatomy. is is a common element used early in the workup of
dysphagia and is a good screening tool. Particular attention
to the morphology of the esophagus (ie, is a sigmoid esophagus present?) and anatomic location of the LES should be
given attention. Classic ndings on barium esophagram
include distal tapering to the GE junction, resulting in a
“bird’s beak” appearance. Air uid levels are often seen (Figs.
14-14 and 14-15). While radiologic reports often will comment on the peristaltic quality of the esophagus, we reserve
such categorization for manometry.
Manometry is used to conrm the diagnosis of achalasia. Aperistalsis of the esophageal body and impaired relaxation of the LES are the hallmark ndings on manometry,
with aperistalsis being a requisite nding. Waveforms are
typically low amplitude and simultaneous (Fig. 14-16).
Vigorous achalasia, a variant in which high-amplitude
waveforms are present can be encountered, and it is usually found in patients with earlier stages of the disease
before complete destruction of the myenteric ganglion
cells ensues.
Endoscopy is an essential part of the workup for achalasia
patients. is oers the chance to directly inspect the mucosa
and evaluate the GE junction. Any abnormalities should
be biopsied to rule out causes of pseudoachalasia, as well as
evaluated with CT and/or endoscopic ultrasound.
304 Part III Esophagus
FIGURE 14-14 UGI demonstrates distal tapering and “bird’s-beak”
appearance in achalasia. (Used with permission from Saurabh
Khandelwal, MD, University of Washington.)
We do not routinely perform 24-hour ambulatory pH
monitoring on these patients, as it does not usually add to the
clinical picture. False-positive results can occur as a result of
fermentation of food within the esophagus.
TREATMENT
erapy for achalasia is palliative in nature and may involve
pharmacologic, endoscopic, and surgical therapies. It must
be emphasized to the patient that therapies do not cure or
address the pathophysiologic abnormality, but instead they
are designed to relieve symptoms of obstruction and impaired
FIGURE 14-15 Sigmoid esophagus seen with long-standing achalasia.
(Used with permission from Saurabh Khandelwal, MD, University of
Washington.)
esophageal emptying by relaxing or disrupting the muscle
bers of the LES.
Medical therapy has focused on drugs that relax
smooth muscle and decrease LES pressure. Nitrates and
calcium channel blockers are used. Because of their limited
eectiveness and inconsistent absorption, their use is limited.
Impaired esophageal emptying can aect their ingestion and
absorption. In randomized controlled trials, calcium channel blockers have not shown signicant success in improving clinical symptoms, despite lowering LES pressures.
50,51
Sildenal, a phosphodiesterase inhibitor, has been shown to
52
have potent relaxing eects on the LES,
but its clinical use is
limited by poor tolerance and side eects. Nitrates, which can
be used in sublingual formulation to overcome poor absorption, tend to work better than calcium channel blockers for
53
symptom relief.
eir use, however, can lead to undesired
side eects such as hypotension and headache and, like all
medical therapies, their ecacy decreases with time. Pharmacologic therapy should be pursued only in patients who, for
medical reasons, are unable to undergo other therapies.
Endoscopic therapies include balloon dilation and botulinum toxin injection. Botulinum toxin injection works by
inhibiting acetylcholine release at cholinergic nerve endings,
thereby decreasing LES pressure. A recent meta-analysis
of therapies for achalasia, by Campos et al, reviewed 315
patients in 9 studies who underwent botulinum toxin
injection and found initial symptom relief of 78.7% at 1
month postprocedure. is steadily declined over time to
40.6% at 12 months, with 46.6% of patients requiring repeat
54
injection.
While botulinum toxin injection therapy may
oer temporary relief of symptoms, its eects are not durable as with surgery and repeat treatments are often needed.
Moreover, when compared with myotomy, the results for
botulinum toxin seem inferior. Zaninotto et al, in a randomized trial comparing botulinum toxin injection with laparoscopic Heller myotomy with fundoplication, observed at 1
year 60% remained asymptomatic in the botulinum injection arm compared with 87% of patients in the surgical arm
being symptom free. At 2 years, only 34% of patients in the
botulinum injection arm remained without symptoms, while
55
87% in the surgical arm remained symptom free.
Multiple
injections can further complicate future surgical therapy due
to the submucosal brosis that can result, making myotomy
56
more dicult and increasing the risk of perforation.
Endoscopic botulinum toxin injection may oer an alternative to
those unwilling or unable to undergo more invasive procedures but has a limited role in the treatment of the disease.
Endoscopic balloon dilation, which creates a controlled
tear in the LES muscle, is another endoscopic therapy that has
been used to treat achalasia and is probably the main alternative to surgery. Dierent types of dilations have been used in
the past, including xed diameter dilators, mercury-weighted
balloons, and water-lled balloons. e most controlled
andconsistent results are seen with the use of noncompliant
pneumatic balloon dilators, such as the Rigiex balloon dilator
57
(Boston Scientic, Boston, MA).
Campos et al, in their
meta-analysis, evaluated 15 studies involving 1065 patients
Chapter 14 Benign Esophageal Disorders 305
Swallow
100
100
100
100
100
100
A
LS
0
0
0
0
0
Nonrelaxation
of the LES
0
4:36.4
LS
LS
Aperistalsis
within the body
30 s
29
27
24
21
18
15
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−3
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B
Swallow
2500
2000
1500
1000
500
0
Ohms
# %
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Aperistaltic
contractions
9
6
3
0
5:17.2
Nonrelaxing LES
30 s
144
119
94
69
44
19
−10
mm Hg
0
7:18.5
FIGURE 14-16 Achalasia as demonstrated by 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.)
306 Part III Esophagus
using new generation pneumatic dilators, and observed symptom relief rates of 84.8% at 1 month postprocedure, 73.8%
at 6 months, and 68.2% at 12 months. After 36 months, the
symptoms relief rate declined to 58.4%. One quarter of all
patients required repeat endoscopic balloon dilation therapy.
54
Balloon dilation has more long-term ecacy than botulinum
toxin injection but still shows signicant rates of symptom
recurrence and the need for repeat therapy. It does carry more
risk than botulinum toxin injection due to the risk of perforation, which is nearly 2% with pneumatic dilation methods.
54
is risk increases with the presence of signicant esophageal
dilation, hiatal hernia, and epiphrenic diverticula (ED). ese
should be considered relative contraindications to pneumatic
dilation. Between the endoscopic therapies mentioned, pneumatic balloon dilation is a more ecacious procedure but
has greater risk of perforation compared to botulinum toxin
injection.
Surgical myotomy was rst described by Ernst Heller in
58
His original description involved performing both an
1913.
anterior and posterior myotomy. is has evolved in most
geal myotomy for achalasia is associated with good longterm results and relief from dysphagia. Long-term follow-up
studies have demonstrated symptom relief in nearly 75%
of patients at 20 years out. Shorter-term follow-up studies
demonstrate that nearly 90% of patients are symptom free
41,54,59
approximately 3 years postprocedure.
Prior hesitancy
for referring patients for Heller myotomy was partially due
to the invasive nature of the procedure, which in the past was
performed via laparotomy or thoracotomy, as well as a long
hospital stay and long recovery. ese approaches eventually
evolved to the minimally invasive approaches via thoracoscopy or laparoscopy. Shimi et al reported the rst laparoscopic
Heller myotomy in 1991, while Pellegrini et al reported the
60,61
rst thoracoscopic approach in 1992.
Drawbacks to this
thoracoscopic approach included the need for single-lung
ventilation, postoperative chest tubes, and being unable to
perform an antireux procedure. e minimally invasive
approach has moved predominantly to the laparoscopic
myotomy approach that has eliminated these drawbacks of
the thoracoscopic approach. Laparoscopy oers excellent
visualization of the hiatus and the mediastinal structures,
does not require single-lung ventilation or postoperative chest
tube drainage, and makes creation of an antireux technically
straightforward. In addition, the laparoscopic performance of
myotomy, when compared with the thoracoscopic technique,
has shown better symptomatic improvement (89.3 vs 77.6%)
and a lower incidence of reux symptoms when combined
with a partial fundoplication (14.9 vs 28.3%).
54
e two main debates surrounding surgical myotomy have
centered on whether or not to include an antireux procedure
(and if so which one) and what the optimal length and extent
of myotomy are that should be performed. GER symptoms
and esophagitis represent common causes of treatment failure
after myotomy if a fundoplication is not added. Addition of an
antireux procedure to a standard Heller myotomy has been
thought to reduce these symptoms and improve outcomes.
is issue has been studied in a prospective, randomized trial
by Richards et al, comparing Heller myotomy with Heller
myotomy plus Dor (anterior) fundoplication. ey demonstrated that the pathologic occurrence of GER, as dened
by distal esophageal acid exposure of greater than 4.2% on
24-hour pH monitoring at 6 months postoperatively, was
reduced from 47.6 to 9.1% with creation of a Dor fundoplica-
62
Some surgeons have advocated in the past for inclusion
tion.
of a oppy Nissen fundoplication, rather than partial fundoplication, to prevent GER. Concern for postoperative dysphagia
due to poor esophageal clearance and weak or absent propulsive force is clearly warranted in this instance. Rebecchi et al
recently published the results of their study in which patients
were randomized to Heller myotomy plus Dor fundoplication or Heller myotomy plus oppy-Nissen fundoplication. At
60months of follow-up, no statistically signicant dierence
in GER symptoms between the two groups were seen; the rate
of dysphagia, however, was found to be signicantly higher in
the oppy-Nissen fundoplication group when compared to the
Dor fundoplication group (15 vs 2.8%). ey concluded that
both antireux procedures oered adequate protection from
GER, but that recurrence of dysphagia was signicantly higher
63
when Nissen fundoplication was performed.
Toupet and Dor
fundoplications with EM are being compared in a randomized,
multicenter trial at this time, and the hope is that the data will
help answer which is a superior antireux procedure. Until the
data can conclusively demonstrate superiority of one technique
over the other, surgeon’s preference and experience should
guide which one is performed in conjunction with myotomy.
e length and extent of myotomy is another area of debate.
Most surgeons agree that the proximal extent of the myotomy
should extend 6–7 cm above the GE junction. is is carried
out in a safe manner with appropriate dissection of the anterior
esophagus. Distally, a standard myotomy has typically been
performed and carried 0.5–1.5 cm below the GE junction.
is length was chosen with the intent of being long enough
to relieve the functional obstruction to the esophagus, while in
64
an eort to preserve an antireux barrier.
e result proved
to fall short on both counts, with dysphagia and/or GERD
being fairly common. In 1998, based on observations that
reoperations for thoracoscopically performed myotomies that
extended the myotomy onto the stomach resulted in improvement of dysphagia, we changed our practice to carry out the
myotomy a full 3 cm below the GE junction (an extended
myotomy) completely obliterating the LES bers. We compared our extended myotomy/Toupet patients with standard
myotomy/Dor patients and observed that patients who underwent extended myotomy had lower LES pressures (9.5 vs 15.8
mm Hg), less frequent and less severe dysphagia, and lower
rates of recurrent severe dysphagia requiring interventions (3 vs
65
We continued to follow and then compared a cohort
17%).
of 52 of these patients at a median follow-up of 46 months.
No signicant dierences in heartburn frequency, esophageal
acid exposure, or LES pressure were observed. However, dysphagia severity was reduced, and relief was improved in the
EM and Toupet fundoplication group. Only 5% of patients
who underwent EM/Toupet required reintervention (dilation)
Chapter 14 Benign Esophageal Disorders 307
versus 18% of SM/Dor patients (10% required endoscopic
66
treatment, 8% required reoperation).
We feel that the Toupet
is a better antireux operation in combination with extended
myotomy. Reasons for its superior ecacy may stem from its
more physiologic angulation of the GE junction with its construction and its ability to stent open the myotomy and prevent
reapproximation of muscle bers and symptom recurrence.
Our study compared two dierent operations (SM and Dor vs
EM and Toupet), and we cannot answer which wrap is superior. At this time, we recommend performing either anterior
or posterior fundoplication with extended myotomy. We continue to routinely perform extended myotomy and have seen
excellent results and low rates of dysphagia. Rarely do we need
to consider dilation, and we have essentially eliminated the
need for reoperation with this approach. Because of this more
complete obliteration of the LES, this should be used in conjunction with an antireux procedure. We feel that extended
myotomy of 3 cm below the GE junction should be a routine
practice when performing a Heller myotomy.
OPERATIVE TECHNIQUE
Laparoscopic Heller Myotomy. e setup is the same as
previously described in this chapter for PEH repair, utilizing
our standard esophageal operating position regarding patient
positioning and trocar placement. We use a 10-mm, 30-degree
laparoscope to ensure the best possible image for performing
the myotomy. is is especially important during the creation
of a myotomy. In contrast, we use 5-mm, 30-degree laparoscopes for PEH repairs and rst-time Nissen fundoplications.
Patients are instructed to remain on a liquid diet for 2 days
prior to surgery to minimize the amount of retained food
within the esophagus and decrease the risk of aspiration at the
time of surgery.
We begin by dividing the phrenogastric ligament sharply
and then divide the short gastric vessels with ultrasonic
shears. A left crus approach is employed as previously
described, and left, right, and anterior mediastinal dissection of the esophagus is performed. It is not necessary to
signicantly dissect the posterior attachments of the esophagus, except to provide enough intra-abdominal esophagus
to perform a good fundoplication. e main goal is to gain
as much length as possible anteriorly to later perform the
myotomy. It is important to identify and preserve the anterior (left) vagus nerve. is nerve and GEJ fat pad are carefully dissected away from the esophageal body and preserved
so that a continuous myotomy can be performed, starting
below on the stomach and extending above the vagus as it
crosses from left to right on the anterior aspect of the GEJ.
e anterior GEJ fat pad to the left of the anterior vagus
nerve is resected. is allows for accurate identication of
the GEJ at the time of myotomy.
At this time, a 50F lighted bougie is passed into the body
of the stomach. e transillumination provided aids in
identication of the submucosal plane. A laparoscopic Babcock clamp, rst applied partially opened over the bougie, is
used to gently drag the tissue over and around the bougie to
provide tension and exposure. e myotomy is started on the
anterior stomach 3 cm below the GEJ. We prefer an L-shaped
hook to perform the myotomy, but other devices can be used
as well. We employ gentle use of cautery to start the myotomy
and then use the L-shaped hook to gently tease the muscle
bers apart, exposing the submucosa. Entering the correct
plane takes patience and careful dissection. e submucosa of
the stomach contains a rich plexus of vessels that can be used
as a visual identier. Once the appropriate plane is identied,
the myotomy is carried cephalad. Only minimal electrocautery is used during performance of the myotomy (Fig. 14-17).
e correct plane may be dicult to identify on the stomach, as the sling bers of the cardia cross in variable directions
and the mucosa tends to be thin. Once the GEJ is reached,
the plane becomes easier to identify due to the organized
outer, longitudinal, and inner circular muscle bers of the
esophagus. We rst divide the outer longitudinal muscle
bers and then the inner circular layer. e myotomy is carefully extended and taken above the level of the anterior vagus
nerve as it crosses from left to right over the esophagus. e
extent of the myotomy is to take it as proximally as is safe.
Typically, one can get 6–8 cm above the GE junction. e
assistant repositions the Babcock clamp as needed to continually provide exposure and tension on the tissues over the
bougie. As the myotomy is carried cephalad, the assistant can
switch over to using an atraumatic grasper to hold the left
side of the divided muscle bers on tension, with the surgeon’s left hand holding the right-sided bers. In this fashion,
the myotomy is completed.
Bleeding from submucosal vessels that are mistaken
for muscle bers occasionally occurs but is self-limited;
gentle pressure is usually adequate to control and stop it.
One must be very cautious in applying electrocautery as an
unrecognized injury may result leading to delayed perforation, and thus should be avoided. If mucosal perforation
occurs during the dissection, it is usually evident as saliva or
gastric secretions or the light from the bougie will be seen
FIGURE 14-17 Myotomy performed over 52F lighted bougie.
(Used with permission from Saurabh Khandelwal, MD, University
of Washington.)
308 Part III Esophagus
coming forth. Intraoperative endoscopy can be used to conrm injury as well as evaluate it after it has been repaired.
Mucosal injuries should be repaired immediately with 4-0
absorbable suture, and consideration given to performing
an anterior, buttressing fundoplication.
Intraoperative endoscopy is carefully performed to evaluate for the completeness of myotomy and to evaluate for
injury. If all muscle bers have been correctly divided, an
open GE junction will clearly be visible on endoscopy, without indentations from undivided bers. In addition, with
gentle insuation, injury to the mucosa can be seen both
endoscopically and laparoscopically.
A Toupet (posterior) fundoplication is performed for the
antireux procedure as the nal part of the operation. A
suture is placed on the posterior portion of the fundus, 3cm
below the GE junction and 2 cm away from the line of the
divided short gastric vessels. is is used as a reference point
to ensure a symmetric posterior wrap. e fundus is brought
posteriorly behind the GE junction, and the reference suture
is grasped and brought up to the edge of the myotomy.
e fundus is sutured to the right crus to alleviate tension,
using 2-0 silk suture. e edge of the wrap is then sutured
to the myotomized edge with three sutures. In similar fashion, the left component of the wrap is sutured to the edge
of the myotomy and the left crus (Figs. 14-18 and 14-19).
FIGURE 14-19 Intraoperative picture of completed Heller myoto-
my with Toupet fundoplication. (Used with permission from Saurabh
Khandelwal, MD, University of Washington.)
After completing the wrap, the ports and liver retractor are
removed and the port sites are closed, concluding the case.
A Dor fundoplication is an acceptable antireux procedure and is technically easier to perform than the Toupet, as
it requires less dissection, especially of the posterior stomach
(Fig. 14-20). e Toupet does a better job of stenting open
the divided muscle bers and with this mechanism may lead
to lower rates of recurrence and dysphagia. For this reason,
we prefer this posterior fundoplication. Figure 14-21 depicts
the construction and geometry of full and partial fundoplications. In patients with a very tortuous or sigmoid shaped
esophagus, we omit the antireux portion of the procedure
because of the high incidence of postoperative dysphagia
we have observed when performing fundoplication in these
patients.
FIGURE 14-18 Diagram of completed Heller myotomy with
Toupet fundoplication. (Woltman TA, Pellegrini CA, Oelschlager
BK. Achalasia. Surg Clin North Am. 2005;85(3):483–493.)
FIGURE 14-20 Completed anterior (Dor) fundoplication. (Used
with permission from Saurabh Khandelwal, MD, University of
Washington.)
Chapter 14 Benign Esophageal Disorders 309
Postoperatively, patients are started on a clear liquid
diet and advanced slowly. We do not use nasogastric tubes.
Nausea is controlled aggressively to prevent retching or emesis. Patients are typically discharged home on postoperative
day 1. On routine follow-up, we assess for symptoms of reux
and dysphagia. At 4–6 months postoperatively, we request
patients to repeat manometry and obtain 24-hour pH testing to evaluate acid exposure. If abnormal acid exposure is
present or the patient has symptoms of GER, a proton pump
inhibitor (PPI) is started to ameliorate symptoms and to
reduce the risk of peptic stricture formation.
A
B
C
FIGURE 14-21 Dierent fundoplication wraps. A. Complete; B. anterior (Dor); C. posterior (Toupet). (Oelschlager B, Eubanks T, Pellegrini C.
Sabiston Textbook of Surgery, 18th ed, Chapter 42.)
310 Part III Esophagus
Summary
Motility disorders of the esophagus share the hallmark
symptom of dysphagia. Careful history taking, in conjunction with physiologic testing with pH and manometry, and
appropriate imaging lead to the diagnosis. With the exception of achalasia, many of these disorders can be managed
medically, especially after careful evaluation and control of
GER. Achalasia is a disease best treated surgically with laparoscopically performed extended myotomy and partial fundoplication. ough endoscopic therapies exist, they have
inferior outcomes and durability, and should be reserved for
patients unwilling or unable to undergo surgery. Minimally
invasive techniques have shown great promise in treating
achalasia both in terms of patient recovery and long-term
outcomes.
ESOPHAGEAL DIVERTICULA
Diverticula of the esophagus are relatively uncommon.
ey are classied based upon their location: proximal
or pharyngoesophageal, midesophageal, and distal or
epiphrenic, with the latter being located within 10 cm of
the GE junction. Midesophageal diverticula, which are
usually traction diverticula and thus are true diverticula,
are rare and usually do not require surgical treatment.
ey result from an extrinsic “pulling” inammatory process and in the past were often associated with tubercular
or granulomatous disease. Proximal and distal diverticula
are more common and are false, or pulsion-type diverticula, as they are not composed of all layers of the esophageal
wall but rather are outpouchings of mucosa. is chapter
focuses on these types, specically Zenker’s diverticulum (ZD) and epiphrenic diverticulum (ED), and their
management.
Zenker’s Diverticulum
Originally described by Ludlow in 1769,67 this proximal
esophageal diverticula was named by German pathologist
Friedrich Albert Von Zenker, who, more than 100 years
later in 1877, described their etiology as being that resulting
from increased pharyngeal pressure leading to formation.
e anatomic location of this lesion is proximal to the upper
esophageal sphincter (UES) and in the posterior hypopharynx. e area in the posterior wall of the pharynx between
the cricopharyngeus muscle and the inferior constrictor muscles is known as Killian’s triangle. e weakest point in this
space is the area between the two muscles, and it is here that
herniation or outpouching of the mucosa and submucosa
occurs, resulting in a Zenker diverticulum (ZD) formation
(Fig. 14-22). In addition to a weak posterior wall, inelasticity
and higher resting tone from brosis of the cricopharyngeus
muscle are thought to contribute to the dysfunction of the
68
Inferior
pharyngeal
constrictor
Killian’s Triangle
Killian-Jamieson Area
Laimer’s Tr iangle
FIGURE 14-22 Schematic drawing of the posterior aspect of the
pharyngoesophageal junction with areas of weakness identied.
Thyroid gland
Cricopharyngeus
Esophagus
Recurrent
laryngeal
nerve
pharyngoesophageal segment, leading to ZD formation.
A complete understanding of the causes for ZD formation
does not exist, despite decades of research.
ZD usually presents in the seventh to eighth decades of
life. It is not uncommon for signicant lengths of time to
elapse between the start of symptoms and presentation to
a surgeon, because the symptoms are often vague, innocuous, with a lot of overlap with other benign conditions. Its
incidence is dicult to estimate as the number of patients
with ZD who are asymptomatic is unknown. Estimates in
the United Kingdom place its incidence at 2 per 100,000
71
population per year.
Common symptoms include dysphagia, globus sensation, halitosis, aspiration, and regurgitation
of undigested food. Physical examination ndings are largely
absent but may infrequently reveal a palpable mass, most
often located in the left side of the neck.
Workup for ZD consists of barium swallow to delineate
size, as measured in the craniocaudal dimension, and position.
Only after this has been done, should endoscopy be attempted
as perforation by blind intubation of the false lumen can lead
to signicant morbidity. Endoscopy largely serves to exclude
other diagnoses, including tumors, mucosal abnormalities,
synchronous esophageal lesions, malignant neoplasia within
the diverticulum, and GERD. Manometry has not shown
specic ndings associated with ZD, though UES dysfunction
may be present.
TREATMENT
erapeutic options have evolved over the last century from
open diverticulectomy and myotomy or diverticulopexy
toward perioral endoscopic methods, including mucomyotomy with staplers, CO
laser, argon plasma coagulation
2
(APC), and needle-knife. No randomized trials have been
conducted comparing the methods. Most methods have
69,70
Chapter 14 Benign Esophageal Disorders 311
comparable symptomatic improvement ranging near or
above 90% and with low morbidity and mortality. Choice
of therapy is often a matter of patient and physician choice.
Trends in therapy, following the European experience, seem
to be shifting toward endoscopic management due to its
low morbidity and mortality, avoidance of an open surgical
69,72
procedure, and good outcomes.
Despite trends toward
endoscopic therapy, there are patients for when the standard
open surgical approach should be used, including those with
narrow mandibles or small oral cavities, those in which the
diverticulum cannot accommodate the scope, and instances
in which the diverticulum is not posterior, for example
73
Killian-Jamieson diverticula.
e instances in which open
surgical resection should always be sought are with diverticula in which mucosal neoplastic changes are known to exist
and those very large diverticula that cannot be approached
safely with a perioral technique.
OPERATIVE TECHNIQUE
Open Cervical Diverticulectomy. Patients with ZD are
placed on a liquid diet for 2 days prior to surgery, to minimize
the risk of retained food and aspiration. e patient is placed
supine with the neck fully extended and the head turned to the
right, exposing the left neck. e left cervical approach is used
as the majority of diverticula occur posteriorly and on the left.
In addition, the esophagus is most accessible here as the trachea
has a natural slight rightward shift. An oblique cervical incision, overlying the anterior border of the sternocleidomastoid
muscle (SCM) is made. e SCM is retracted laterally as is the
carotid sheath, while the thyroid gland is retracted medially.
Ligation of the middle thyroid vein and omohyoid muscle is
necessary to gain medial retraction of the thyroid and exposure
of the tracheoesophageal groove and esophagus. e left recurrent laryngeal nerve should be identied and preserved. A leftsided approach is also more desirable from this aspect as the
recurrent laryngeal nerve on this side has better exposure and
more consistent anatomy compared to the right.
Dissection is carried distally and cephalad. A true ZD will
be encountered in the posterior midline at Killian’s triangle;
it is grasped and its neck is dissected free. Next, a 50F bougie is placed under palpation and direct vision of the surgeon
into the distal esophagus. A myotomy is performed, which
must include the cricopharyngeus muscle and come down
several centimeters onto the esophagus, which can be identied by its outer longitudinal and inner circular muscle bers.
e diverticulum is excised using a reticulating linear stapler
(Fig. 14-23A–C). Resection of the diverticulum should be
performed with the bougie in place to avoid narrowing of the
esophagus. A drain may be placed at the discretion ofthe surgeon. e platysma is closed and the wound is closed in layers.
If the patient is doing well clinically, he or she is started on a
liquid diet the next day and can be discharged within 48 hours.
Surgical open diverticulectomy and myotomy are associated with excellent relief from symptoms in up 82–94% of
69
patients and low recurrence rates of 3.6–7%.
Mild to severe
complications, including staple-line leak, stula formation,
stenosis, recurrent laryngeal nerve palsy, mediastinitis, pneumonia, and hemorrhage have an occurrence rate of up to
25%. Mortality associated with the surgical approach ranges
between 1.2 and 3.4%.
69,74–78
Endoscopic Treatment. Endoscopic treatment of ZD
79
was rst described by Mosher
in 1917 and lost favor,
because of complications, until revived by Dohlman and
80
Mattsson in 1960.
ey reintroduced the concept with
use of electrocoagulation techniques. Collard et al in 1993
described the endoscopic stapled diverticulectomy (ESD)
that is the predominant endoscopic method of treatment
81
today.
Endoluminal treatments for ZD are the least invasive methods of treatment and the various forms all share
the common principle of performing mucomyotomy by
dividing the septum between the diverticulum and the
esophageal lumen. CO
clips, and staplers have been described and used.
laser, electrocautery, needle-knife,
2
80–83
e
stapled diverticulectomy oers the additional advantage
over these other methods of wound closure with the staples
after division of the septum is completed. is is thought
to decrease the risk of bleeding and possible perforation.
Both rigid and exible endoscopy platforms can be used.
Rigid endoscopy is usually performed in the operating
room by ENT (ear, nose, and throat) surgeons, and it
incorporates the use of the stapler and a diverticuloscope,
which can intubate both the esophageal lumen and diverticulum simultaneously (Fig. 14-24). Flexible endoscopic
techniques employ various methods of cautery, cutting or
clipping, or laser to divide the septum. Flexible endoscopy
oers some advantages over the rigid method in that it can
be done with sedation and analgesia, avoiding a general
anesthetic, and can be performed in an outpatient setting
with reduced stay and potential cost savings. It is associated
with higher recurrence rate when compared to rigid endoscopy and ESD (up to 35% in some series vs up to 15.4%
for ESD and rigid endoscopy). Head-to-head randomized
trials comparing the diering endoluminal approaches
have not been performed.
Endoluminal therapies demonstrate excellent symptom
improvement in 80–96% of patients. Mild complications
such as subcutaneous emphysema or mild hemorrhage are
seen in up to 23% of patients; severe complications occur
less frequently when compared to surgical treatment, ranging
69,84
from 0 to 3.8%.
e most feared of these are esophageal
or pharyngeal perforation. Mortality rates are low (0–0.4%)
and no mortalities have been reported with the exible endoscopic methods. Recurrence rates, however, are signicantly
higher than with surgical therapy and range between 3.3 and
69
Between the methods, the exible platform has the
35%.
highest recurrence rates; this can often be addressed with
repeat therapy. While this is a drawback, the overall safety
and lower-risk prole of endoluminal therapies may be a
desirable factor when treating elderly patients, in which ZD
most commonly presents. All patients are not candidates for
endoluminal treatment of ZD, such as those with small oral
cavities, large osteophytes, and small diverticula (<3 cm).
73