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312 Part III Esophagus
52F
A
Bougie
Planned site of myotomy
B
C
FIGURE 14-23 A. Zenker’s diverticulum, dashed line indicates proposed site of myotomy. B. Isolation of Zenker’s diverticulum, with myotomy.
C. Resection of Zenker’s diverticulum with gastrointestinal anastomosis (GIA) stapler.
Small diverticula are dicult to engage with the stapling device and diverticuloscope.
endoscopy) are employed. All therapies are associated with greater than 90% symptom relief. Endoscopic therapies are associated with shorter length of stay, can be performed as outpatient procedures, and may avoid general anesthetic
Summary
administration. However, they are associated with higher recurrence rates, which can often be addressed with repeat
ZD is a rare disorder in which a pulsion-type diverticulum occurs in the posterior pharyngoesophageal region. Both surgical and endoscopic treatments (using rigid or exible
endoscopic treatment. ese are important factors to con­sider as ZD usually presents in elderly patients who are more likely to be inrm. Both open surgical technique and perioral
Chapter 14 Benign Esophageal Disorders 313
A
Diverticuloscope
Diverticulum
B
Endo GIA
Copyright © 2002, University of Washington. All rights reserved.
FIGURE 14-24 Zenker’s diverticulectomy using diverticuloscope and stapler to perform mucomyotomy.
endoscopic methods are valid treatment methods and the choice of which to pursue should be based upon anatomic considerations, available expertise, and patient comorbidities.
disorder. Assuch, these patients may present with symptoms similar to the aforementioned motility disorders, most com­monly to include dysphagia, chest pain, heartburn, and regur­gitation. Intermittent nocturnal aspiration is frequently seen and occurs in nearly 45% of patients.
Epiphrenic Diverticula
patients should include a complete history and examination, upper GI barium swallow, esophageal manometry and pH
Diverticula present in the distal third of the esophagus, usually within 10 cm of the GE junction, are referred to as epiphrenic diverticula (ED). It is a rare condition, and its true incidence remains unclear as the number of patients with asymptomatic diverticula is not known. ese are pulsion-type false divertic­ula, similar to ZD, as they are only outpouchings of mucosa and submucosa through the muscular wall of the esophagus. e pathophysiology underlying the disease, rst recognized
85
by Mondiere in 1833,
is assumed to be elevated esophageal
testing, and endoscopy (Fig. 14-25). Some controversy exists regarding who should be treated surgically. ose with mild symptoms and small-size diverticula, or those to whom surgery presents signicant risk, can be safely observed. If symptoms of GERD are present, they may be controlled with medications. ese patients should be followed for progression of their symp-
90
ose with severe symptoms who are candidates for sur-
toms. gery should be treated surgically.
intraluminal pressures, as a result of an underlying esophageal motility disorder, in conjunction with functional distal obstruc­tion. With the advent of esophageal manometric testing, it is
Treatment
clear that EDs are commonly associated with a heterogeneous group of motility disorders and LES dysfunction, including achalasia, DES, Nutcracker esophagus, hypertensive LES, as well as nonspecic esophageal motility disorders (NSMD),
86,87
although often there is no detectable underlying motility
Surgical treatment focuses on the concepts of resection of the diverticulum and treatment of the underlying esopha­geal motility disorder to relieve the functional obstruction, typically with long esophagogastric myotomy. Historically,
88,89
e workup of these
314 Part III Esophagus
FIGURE 14-25 Upper GI Barium study. Arrows demonstrating
two epiphrenic diverticula. (Used with permission from Saurabh Khandelwal, MD, University of Washington.)
this was performed through a left thoracotomy to provide optimal exposure to the distal esophagus, GE junction, and
91
cardia.
is was associated with excellent symptom relief in 76–94% of patients, but with mortality rates of up to 15% and complication rates of nearly 40%. Leak rates of
92–94
6–18% were observed.
Just as with treatment of acha­lasia and other benign esophageal disorders, the dominant operative technique has now shifted to the minimally inva­sive approach. Both the video-assisted thoracoscopic surgery (VATS) and laparoscopic approach have been described
95,96
neither these nor the open approach have been compared in a randomized prospective fashion. When compared to thora­cotomy approach, both minimally invasive techniques (VATS and laparoscopy) are associated with lower perioperative mor­tality rates (0–7.7%), shorter length of stay, and lower leak rates (14% cumulative rate); morbidity still ranges as high as
94,97,98
50%. lent relief of symptoms is seen in 83–100% of patients.
With the minimally invasive approaches, excel-
94
e laparoscopic approach, which has been the minimally invasive technique predominantly reported, capitalizes on these advan­tages and avoids single-lung ventilation and postoperative chest tubes. In addition, performing fundoplication is techni­cally easier with the laparoscopic approach compared to the VATS approach. e laparoscopic method is the one we have adopted, in which we perform stapled resection of the diver­ticulum, long myotomy, and Toupet fundoplication.
Operative Technique
LAPAROSCOPIC EPIPHRENIC DIVERTICULECTOMY
Patients are placed on a liquid diet for 48 hours prior to operation to minimize retained food in the diverticulum.
At the time of operation, endoscopy is performed prior to commencing, while the patient is under general anesthetic, to remove any retained debris and avoid its incorporation into the eventual suture line. e standard esophageal operating position is used, as previously described in this chapter. A 10-mm, 30-degree laparoscope is used to obtain the best image, and a liver retractor is placed to visualize the hiatus. e short gastric vessels are ligated, and the left crus technique is used to begin the division and dissection of the phrenoesophageal membrane. A Penrose drain is placed around the esophagus to aid with retraction. e esophagus is circumferentially dissected up into the mediastinum. e diverticulum usually becomes apparent at this time. Most diverticula are encountered on the right side. e diver­ticulum is freed from surrounding structures and dissected using both blunt and sharp dissection, taking care to cleanly expose the neck. e least obvious, but most important aspect of this is separating the diverticulum from the sur­rounding esophagus by dividing adhesions connecting the two. is is often underappreciated and can lead to incom­plete resection of the diverticulum. An appropriately sized bougie is carefully placed in the esophagus (50–60 F) ensur­ing it does not enter the mouth of the diverticulum. e diverticulum is resected using an articulating laparoscopic stapling device, keeping the stapler parallel to the esopha­gus and using the bougie for guidance and to help avoid narrowing (Figs. 14-26A–C). e laparoscopic approach typically aords better visualization and stapler alignment than either VATS or open thoracotomy. e stapled edge is inspected to make sure there is no bleeding or disrup­tion. A myotomy is performed opposite the suture line in the same fashion as previously described for achalasia, with extension of 3 cm onto the cardia. e separation of muscle
;
bers from the myotomy allows the suture line to be over­sewn in Lembert fashion using interrupted sutures placed in intracorporeal fashion to protect it. Finally, a Toupet fundo­plication is then performed as previously described to com­plete the operation, which provides protection from GER and in most cases will buttress the staple line. Endoscopy is performed to evaluate for leak or narrowing. Patients are admitted and an UGI barium study is performed on post­operative day 2. If no leak or stricture is seen, the patient is started on liquids and discharged home.
Summary
Epiphrenic diverticula are a rare type of pulsion diverticula that occur in the distal third of the esophagus. Treatment should be oered to those with symptomatic diverticula who are medically t for surgery. erapy should include surgical resection of the diverticulum and address the motility disorder to provide relief of distal obstruction, typically with long myotomy. Minimally invasive meth­ods with either VATS or laparoscopy have demonstrated excellent symptomatic relief and lower mortality and mor­bidity compared to the older approach with thoracotomy.
Chapter 14 Benign Esophageal Disorders 315
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GASTROESOPHAGEAL REFLUX DISEASE AND HIATAL HERNIA (INCLUDING PARAESOPHAGEAL)

Toshitaka Hoppo Shamus R. Carr Blair A. Jobe
15
GERD—OVERVIEW
De nition
Gastroesophageal re ux disease (GERD) is a chronic disor- der related to the retrograde  ow of gastric contents into the esophagus, resulting in a spectrum of symptoms with or without tissue injury. absence of esophageal mucosal complications are the hall­marks of nonerosive re ux disease (NERD). Patients with NERD account for up to 70% of those with GERD in the community. long-term therapy. Although various endoscopic approaches to treat GERD have been introduced, none of them has been able to achieve an e cacy equivalent to antire ux surgery.
2
Antire ux surgery is the only e ective and
3,
4
1
Classic GERD symptoms in the
Symptoms
Heartburn (ascending retrosternal burning) and regurgita­tion are typical GERD symptoms. Epidemiologic studies have demonstrated that heartburn occurs monthly in as many as 40–50% of the Western population.  e occur­rence of heartburn at night and its e ect on quality of life have recently been highlighted by a Gallup poll conducted by the American Gastroenterologic Society ( Table 15-1 ). Regurgitation of gastric contents often occurs when the patient is supine or with increases in intra- abdominal pres­sure, and may result in atypical symptoms, including cough, globus sensation, hoarseness, throat clearing, asthma, aspi­ration pneumonia, and pulmonary  brosis. Dysphagia is a typical symptom of GERD and can be divided into (1) an oropharyngeal etiology, which is characterized by di culty
5
transferring food out of the mouth into the esophagus, and (2) esophageal etiology, which is characterized by the sensation of food sticking in the lower chest. Dysphagia can be a sign of underlying malignancy and should be aggres­sively investigated with upper endoscopy. Chest pain can be caused by GERD; however, it is very important to exclude a cardiac etiology. DeMeester and colleagues reported that nearly 50% of patients with severe noncardiac chest pain had a positive 24-hour pH study implicating GERD as the underlying etiology. occurring at night while supine, nonradiating, responsive to antacid medication, or accompanied by other symptoms such as dysphagia and/or regurgitation should trigger an evaluation for an esophageal cause. Additionally, it should be noted that the distinction between heartburn and chest pain can be di cult to make, and the perception of these symptoms is highly variable between patients.
6
Chest pain precipitated by meals,
7,
PATHOPHYSIOLOGY OF GERD
 e antire ux mechanism includes four important components: (1) lower esophageal sphincter (LES); (2) crural diaphragm; (3) esophageal peristalsis; and (4) stomach (the reservoir).
Lower Esophageal Sphincter
 e gastroesophageal junction (GEJ) is a complex arrange- ment of specialized muscles composed of both intrinsic (LES) and extrinsic (crural diaphragm) contractile elements.  e LES, which can be identi ed as a high-pressure zone located at the GEJ, creates the barrier between the esopha­gus and stomach that normally prevents re ux. LES relax-
8
319
320 Part III Esophagus
TABLE 15-1: AMERICAN GASTROENTERO-
LOGIC ASSOCIATION GALLUP POLL ON NIGHTTIME GASTROESOPHAGEAL REFLUX DISEASE SYMPTOMS
•  • 
both day and night
• 
work the next day
•  • 
symptoms
ation occurs in two situations: (1) immediately following a swallow, when it momentarily relaxes to allow passage of food into the stomach, and (2) when the fundus is distended with gas, it is eliminated to allow venting of the gas (a belch)—tran­sient LES relaxation (TLESR). For an LES to be e ective, it must possess three characteristics: an adequate (1) total length, (2) intra-abdominal length, and (3) resting pressure
9
( Table 15-2 ).
 erefore, a defective LES is identi ed by one or more of the following characteristics: (1) a high-pressure zone with an average pressure of less than 6mm Hg, (2) an average overall length of 2 cm or less, and (3) an average length exposed to the positive pressure environment of the abdomen (intra-abdominal length) of 1 cm or less.  e most common cause of a permanently defective LES is an inade­quate abdominal length, secondary to the high prevalence of
9
a hiatal hernia in patients with GERD.
A TLESR is an LES
relaxation that occurs without a swallow and accounts for the physiologic re ux and “venting” of the stomach, particularly in the postprandial state. Frequent and prolonged TLESR can be associated with the development of GERD, and this may explain the etiology of disease observed in the 40% of patients with a manometrically normal sphincter. A transient loss of the LES can also occur due to a functional problem of
10
the gastric reservoir and delayed emptying.
In this setting, if excessive air and food are swallowed, there are gastric disten­tion and an increase in intra-gastric pressure with shortening of the LES ( Fig. 15-1 ).  is process continues until a criti­cal LES length is reached and eventually the pressure drops precipitously and re ux occurs.  is “transient sphincter”
TABLE 15-2: NORMAL MANOMETRIC
VALUES OF THE LOWER ESOPHAGEAL SPHINCTER, N = 50
shortening occurs in the initial stages of GERD and is the mechanism for the early complaint of excessive postprandial re ux.  is process is associated with the common com­plaints of belching and bloating in patients with GERD. To compound matters, there is an increased frequency of swal­lowing (air and saliva) observed in GERD patients because the ingestion of saliva (pH 7) serves to neutralize the acidic
11
 uid (pH 1) in the esophagus.
 erefore, GERD may begin in the stomach, secondary to gastric distention due to overeating and a high-fat diet, which delays gastric emp­tying. Further, a close relationship between the geometry of the cardia and one’s propensity to re ux in the face of
10
a given intragastric pressure has been established.
Greater gastric distension, as re ected by an increasing intragastric pressure, is necessary to “open” the sphincter in patients with an intact angle of His compared to those with hiatal
12
hernia ( Fig. 15-2 ).
 ese data elucidate why the presence of a hiatal hernia is often associated with GERD and explain the loss of the  ap valve mechanism (intragastric portion of LES). In addition, in the presence of a hiatal hernia the intrinsic portion of the LES is no longer aided by the crural diaphragm (extrinsic LES).
Esophageal Peristalsis
Esophageal peristalsis is an extremely important component of the antire ux mechanism and serves to clear physiologic re ux and thus reduces contact time between the esophageal epi­thelium and gastric  uid. Ine ective esophageal motility can result in an abnormal esophageal exposure to gastric juice even in individuals with a mechanically e ective LES and normal gastric function. seen in patients with a mechanically defective LES, where dis­tal esophageal body function deteriorates as a direct result of repetitive in ammation; this e ect further prolongs the esoph­ageal exposure to gastric juice, which creates a vicious cycle leading to more severe disease. Diener and colleagues reported that 40–50% of patients with GERD had abnormal esopha­geal peristalsis. was prolonged, and gastric  uid was in contact with the esoph­ageal mucosa for a longer period of time and traveled more proximally when compared to GERD patients with intact esophageal motility.  erefore, these patients were prone to having more severe mucosal injury and extraesophageal symp­toms such as cough. lished that patients with mixed connective tissue diseases such as scleroderma commonly have an aperistaltic esophagus and absent LES, which results in the most severe form of GERD.
13
However, ine ective motility is more often
13
In these patients, esophageal clearance time
14,
15 To highlight these points, it is estab-
16
Parameter
Pressure (mm Hg) 13 5.8 27.7 Overall length (cm) 3.6 2.1 5.6 Abdominal length (cm) 2 0.9 4.7
Median value
2.5th percentile
97.5th percentile
Crural Diaphragm
 e crural diaphragm provides an extrinsic component to the gastroesophageal barrier. Mittal and colleagues demon­strated a direct correlation between intraluminal pressure of the GEJ and integrated electrical activity of the crural
Chapter 15 Gastroesophageal Reux Disease and Hiatal Hernia (Including Paraesophageal) 321
B
A
C
FIGURE 15-1 A graphic illustration of the shortening of the lower esophageal sphincter that occurs as the sphincter is “taken up” by the cardia
as the stomach distends.