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ESOPHAGUS
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7
Surgical Management of Gastroesophageal Reflux Disease
Jay Zhu, MD, and Brant K. Oelschlager, MD
astroesophageal reflux occurs when the contents and secretions of the stomach flow retrograde into the esophagus across an
G
inappropriately relaxed or compromised lower esophageal sphinc­ter. Although nearly everyone experiences symptomatic episodes of reflux to some degree in their lifetime, gastroesophageal reflux disease (GERD) is a condition characterized by chronic symptoms or complications related to gastroesophageal reflux. GERD is a com­mon diagnosis, affecting up to 20% to 30% of the US population and costing an estimated $12 billion to $20 billion in direct healthcare expenditure annually. The high incidence of GERD in the United States and other Western countries is also thought to be the primary reason behind the rising incidence of esophageal adenocarcinoma over the past four decades. In this chapter, we discuss the surgical evaluation and technical approach to gastroesophageal reflux disease.
PRESENTATIONS OF GERD
Symptoms related to GERD can be divided into typical, atypical, and alarm symptoms (Box 1). Typical symptoms of GERD are the classic esophageal manifestations of gastroesophageal reflux, which include heartburn and regurgitation. Atypical symptoms encom­pass the extraesophageal manifestations of reflux such as cough, dysphonia, sore throat, globus sensation, and noncardiac chest pain. Although GERD can be clinically diagnosed in patients presenting with typical symptoms, patients presenting primarily with atypical symptoms require further investigation to rule out other causes. For surgeons, distinguishing typical from atypical symptoms is useful in assessing the likelihood that a patient’s symptoms are attributable to GERD and thus will respond to surgical intervention. Patients with heartburn and regurgitation tend to be more responsive to
acid suppression therapy and experience higher rates of symptom resolution after antireflux surgery (ARS) when compared with those presenting with atypical symptoms.
Alarm symptoms are ones that raise suspicion for malignancy and other complications of GERD. These include weight loss, early satiety, dysphagia, odynophagia, and signs of gastrointestinal bleed­ing. Alarm symptoms should never be attributed solely to uncompli­cated GERD, and patients presenting with these symptoms require further workup. The chronic inflammation and irritation associated with reflux can lead to intraesophageal complications such as peptic stricture, Barrett’s metaplasia, and esophageal adenocarcinoma. Less commonly, reflux can also lead to extraesophageal complications such as laryngopharyngeal reflux and lung injury from aspiration. Exacerbations of asthma or interstitial lung diseases are unusual manifestations of GERD but clear reasons to consider surgical inter­vention. It is important to mention that decisions regarding ARS in patients with complications of GERD are often shared across disci­plines. When treating patients with GERD-related complications, we often work closely with colleagues in gastroenterology, otolaryngol­ogy, or pulmonology depending on the specific complication.
DIAGNOSIS AND PREOPERATIVE
EVALUATION
The primary purpose of preoperative of testing in the surgical evalua­tion of GERD is to (1) confirm the correct diagnosis, (2) evaluate the anatomy (e.g., the presence of a hiatal hernia), and (3) rule out con­current esophageal or gastric pathology before surgery. We routinely obtain the following tests before surgical consultation for GERD.
pH testing: Ambulatory pH monitoring in patients off acid
suppression therapy is the gold standard for diagnosing GERD.
This is accomplished using either a 24-hour dual-probe catheter
system placed transnasally or a 48-hour wireless capsule placed
endoscopically. Both tests rely on correct spacing above the lower
esophageal sphincter and generate a composite score based on the
frequency and duration of distal esophageal acid exposure (i.e.,
pH below 4). A DeMeester composite score above 14.72 or total
distal esophageal acid exposure time greater than 5% to 6% are
commonly used thresholds indicative of pathologic reflux.
Upper endoscopy: The presence of LA Grade C or D esophagi-
tis (Table 1; Fig. 1), Barrett’s metaplasia, or a peptic stricture on
BOX 1 Presenting Symptoms of Gastroesophageal
Reflux
Typical Symptoms
Heartburn (also known as pyrosis) Regurgitation Acid brash
Atypical Symptoms
Cough Wheezing Dyspnea/shortness of breath Voice changes Sore throat Globus sensation
Alarm Symptoms
Dysphagia Odynophagia Anorexia/early satiety Weight loss Gastrointestinal bleeding
TABLE 1 The Los Angeles Classification of
Esophagitis
Grade Lesion
A One (or more) mucosal break <5 mm long
that does not extend between the tops of two mucosal folds
B One (or more) mucosal break >5 mm long
that does not extend between the tops of two mucosal folds
C One (or more) mucosal break that is con-
tinuous between the tops of two or more mucosal folds but that involves <75% of the circumference
D One (or more) mucosal break that
involves at least 75% of the esophageal circumference
8 SURGICAL MANAGEMENT OF GASTROESOPHAGEAL REFLUX DISEASE
Grade A
Grade C
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Grade B
Grade D
FIG. 1 The Los Angeles classification of esophagitis. Grades A to D are illustrated as described in Table 1. (From Nayar DS, Vaezi MF. Classifications of esophagi-
tis: Who needs them? Gastrointest Endosc. 2004;60[2]:253–257.)
endoscopy are all findings that confirm the diagnosis of GERD. In the case of peptic strictures, serial endoscopic dilations can pro­vide therapy before ARS. Furthermore, endoscopic examinations are useful in identifying hiatal hernias, retained food suggestive of delayed gastric emptying, and other gross pathology involving the esophagus and stomach.
Manometry: We use esophageal manometry in the setting of
GERD primarily to help determine the type of fundoplication to perform. Our preference is to perform a complete 360-degree posterior (Nissen) fundoplication for patients who exhibit nor­mal esophageal motility as this is likely the most durable treat­ment for reflux. For patients who have ineffective esophageal motility according to Chicago Classification version 4.0 (updated in 2020), we consider performing a partial 270-degree posterior (Toupet) fundoplication to avoid issues with postoperative dys­phagia. Obtaining a manometry study also serves to rule out achalasia and other named esophageal motility disorders, which can sometimes present with symptoms that overlap with GERD.
Barium Esophagram: Combined with the aforementioned stud-
ies, an upper GI barium esophagram increases the sensitivity of diagnosing a hiatal hernia or identifying other anatomic abnor­malities such as an esophageal diverticulum. This is especially relevant when the treating surgeon is not the one performing the preoperative endoscopy. Furthermore, a high-quality barium esophagram is particularly useful in understanding the anatomy and geometry of a previously constructed wrap in patients with postoperative concerns or complications.
INITIAL MANAGEMENT AND INDICATIONS FOR SURGERY
With rare exception, all patients should be on acid suppression therapy with a proton pump inhibitor (PPI) before being considered for ARS. It is important to ensure that patients are taking PPIs con­sistently and correctly (usually 40 mg daily) to maximize the drug’s efficacy and assess for a clinical response in symptoms. In general, PPIs are well-tolerated, and adverse reactions or side effects such
as nausea, diarrhea, constipation, and abdominal discomfort are rare. Patients who report preoperative issues with bloating may be evaluated for delayed gastric emptying and should be counseled on the risk of worsening gas bloat when weighing the risks and benefits of ARS.
Indications for Surgical Management of GERD
The primary reason to perform ARS is for symptomatic control to reduce suffering and improve patients’ quality of life. Fundoplication has not been shown to reduce rates of esophageal adenocarcinoma or improve survival outcomes. Accordingly, the most common indica­tion for ARS is the presence of persistent symptoms that affect qual­ity of life despite maximal medical therapy. As previously discussed, patients who exhibit atypical or alarm symptoms should undergo appropriate workup and/or interdisciplinary consultation as indi­cated. In patients with atypical symptoms and objectively confirmed reflux, we estimate that approximately one-third of these patients may not see improvement in their symptoms following ARS. Thus, it is important to counsel such patients carefully when weighing the risks and benefits of an operation. In general, patients presenting with typical GERD symptoms that are partially mitigated with acid suppression (or worsen when stopping acid suppression) are most likely to experience significant improvement following ARS.
Although the inability to tolerate acid suppression therapy is an indication for surgical management, true medication intolerance in the treatment of GERD should be rare. More commonly, patients will present with hesitancy or concerns surrounding long-term acid suppression therapy, with many seeking a definitive solution to their reflux. In patients who have well-controlled symptoms on a PPI, we typically advise against surgical intervention because the risks and side effects of ARS outweigh the risks of regular acid suppression therapy. Stated differently, it is very difficult to improve upon medi­cally well-managed symptoms through an operation.
Finally, some patients with interstitial lung disease and objective findings of GERD may benefit from ARS. Data suggest that ARS can slow the deterioration of pulmonary function in these patients,
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which can be particularly relevant for patients who are either being considered for lung transplantation or have already undergone trans­plantation. The decision and timing of ARS in this setting should be made in discussion with the patient’s pulmonologist.
Contraindications to Antireflux Surgery
Patients with a normal DeMeester score and normal distal acid exposure on ambulatory pH testing should not be considered for ARS. Symptomatic patients who do not demonstrate objective find­ings of abnormal reflux should undergo further workup to identify an alternative diagnosis. The use of impedance or pharyngeal pH monitoring to confirm pathologic GERD is controversial and should be evaluated with caution. On the other hand, patients may have abnormal ambulatory pH monitoring, but complete preoperative workup demonstrates another diagnosis altogether such as achalasia, esophageal cancer, or a large paraesophageal hernia. In these cases, the primary diagnosis is not GERD, and patients should be treated appropriately for these other disorders. Finally, obesity is a relative contraindication for ARS. Patients with a BMI >40 should be referred for bariatric surgery evaluation to be considered for Roux-en-Y gastric bypass, as this procedure addresses the broader spectrum of obesity-related health problems, which includes GERD.
SURGICAL TECHNIQUE
In 1937, Rudolf Nissen performed the first known fundoplication in which he wrapped the stomach to buttress an esophagogastric anastomosis as part of the repair for a penetrating esophageal ulcer. Later in the 1950s, he utilized this technique for the first time as a treatment for reflux. Since then, the eponymous 360-degree wrap has become the gold standard in ARS. Although advances in technology have introduced laparoscopic and robotic-assisted approaches to ARS, the surgical principles remain the same with the goal of restor­ing intraabdominal esophageal length, closing the hiatal defect, and creating a one-way flap valve. Newer endoscopic approaches such as the transoral incisionless fundoplication only accomplishes one of these three goals, and long-term outcomes are still unknown. Here, we describe a laparoscopic Nissen fundoplication, which continues to be our favored procedure for GERD, and a laparoscopic Toupet fundoplication, which we perform in patients with ineffective esoph­ageal motility (Fig. 2).
Steps of the Procedure: Initial Setup, Hiatal Dissection, and Closure of the Crura
The initial steps in performing a laparoscopic fundoplication are similar, regardless of whether a partial or complete fundoplication is being constructed. We use the same instruments (Box 2), patient positioning, and port placement (Fig. 3) for both a Nissen and a Toupet fundoplication. Although the hiatal dissection can begin on either side of the gastroesophageal junction, we prefer to first expose the left crus and then enter the mediastinum starting on the left, as follows.
1. Patient positioning and port placement a. The patient is positioned supine in the split leg position with
padded straps secured around both thighs (some prefer litho­tomy). The surgeon stands between the patient’s legs while the assistant stands on the left side of the patient. Before draping, the operating table should be tested in the steep reverse Tren­delenburg position in which the procedure is performed to ensure that the patient is secure and not at risk of shifting or sliding during the operation.
b. A Veress needle is used to access and insufflate the abdomen,
and the ports are placed as shown in Figure 3. The patient is then placed in steep reverse Trendelenburg before elevating the left lateral segment of the liver using a liver retractor
(we use a Nathanson retractor). We typically use a 5-mm 30-degree scope.
2. Exposing and opening the hiatus on the left side (note that some prefer to start on the right) a. The fundus is retracted caudally to expose the membranous
avascular phrenogastric attachments between the fundus and the diaphragm. These attachments are divided to begin expo­sure of the left crus.
b. The gastrosplenic ligament is divided near the inferior pole of
the spleen to enter the lesser sac. The gastrosplenic ligament and the associated short gastric vessels are then divided with a vessel-sealing energy device to mobilize the fundus. The pos­terior attachments of the stomach are divided to ensure that the fundus is completely mobilized.
c. With the fundus retracted medially, the left crus should
be clearly exposed. Additional medial traction on the gas­troesophageal junction places the phrenogastric ligament on tension, exposing this white membranous connection between the medial border of the left crus and the intraab­dominal esophagus. This membrane is carefully divided at the posterior base of the left crus, opening a space to the left of the esophagus. The correct mediastinal plane contains thin areolar connective tissue that can typically be easily developed with blunt dissection using the tip of a suction device or other instrument. Once the correct plane is identified, the left phren­oesophageal membrane is continually placed on stretch as it is divided, progressing anteriorly and sweeping tissue away from the membrane toward the esophagus to avoid injury to the anterior vagus nerve. Care is taken not to denude the perito­neum off the crus, as this can weaken the crural closure.
d. A blunt instrument can then be inserted behind the esophagus
to create a retroesophageal window from the left side.
3. Exposing and opening the hiatus on the right side a. The gastrohepatic ligament is divided starting at the pars
flaccida and continuing cephalad toward the anterior aspect of the esophageal hiatus to expose the right crus. If a sizeable accessory or replaced left hepatic artery is encountered, this should be preserved.
b. The retroperitoneal fat attached to the right crus above the
left gastric artery can be retracted toward the patient’s left to expose the right phrenoesophageal membrane. This should be divided to enter the same mediastinal plane that was devel­oped on the left. The dissection can then be carried out cir­cumferentially in similar fashion as on the left side, following the same principles of preserving the peritoneal covering over the right crus while bluntly sweeping tissue toward the esoph­agus to identify and preserve both anterior and posterior vagal nerves (Fig. 4).
c. Once the phrenoesophageal membrane has been circumferen-
tially opened around the esophagus, a ½-inch Penrose drain is inserted and encircled around the gastroesophageal junction, and then secured to itself using either suture or clips. This provides the assistant a handle to retract the esophagus during mobilization of the distal esophagus.
4. Distal esophageal mobilization a. The dissection is carried circumferentially around the esoph-
agus, identifying and preserving both vagal nerves as the dissection progresses up into the mediastinum. Direct arterial branches from the aorta to the esophagus can be ligated using a vessel-sealing energy device. Care should be taken to avoid dissecting into the retroperitoneal fat overlying the aorta, as this is where the thoracic duct resides.
b. The parietal pleura when identified should be swept laterally
to avoid injury and creation of a capnothorax. If the pleura is entered inadvertently, it is important to communicate this finding with the anesthesia provider. If the opening in the pleura is easily identified, we typically choose to close
10 SURGICAL MANAGEMENT OF GASTROESOPHAGEAL REFLUX DISEASE
C
AB
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Wrap
Esophagus
Wrap
Esophagus
180˚
140˚± 20
Esophagus
Wrap
FIG. 2 The most common types of fundoplication. (A) 360-degree
Nissen fundoplication. (B) 180-degree anterior Dor fundoplication. (C) 270-degree posterior Toupet fundoplication. (From Yates RB, Oelschlager BK,
Pelligrini CA. Gastroesophageal reflux disease and hiatal hernia. In Townsend etal., eds. Sabiston Textbook of Surgery. 20th ed. Philadelphia: Elsevier; 2017:1043–
1064.)
derangements associated with a capnothorax. However, when closure of a pleural defect is not easily achievable, expectant management and lowering of the intraabdominal insufflation pressure will typically suffice as this allows the patient to compensate physiologically for the carbon dioxide introduced into the hemithorax. Usually after a few minutes, parameters such as decreased blood pressure, increased ventilatory pres­sure, and increased end-tidal CO surgeon to proceed with the operation.
c. The lower esophagus should be mobilized to achieve 3 to 5 cm
of intraabdominal length without tension.
will stabilize, allowing the
2
5. Closure of the crura a. Nonabsorbable suture is used to reapproximate the crura
posterior to the esophagus. We prefer to use interrupted 2-0 silk without pledgets. This closure is performed until the esophageal hiatus approximates the diameter of the esophagus without any notable gaps. At the same time, the hiatal closure should not apply any external compression on the esophagus.
b. On rare occasion, we will place a single anterior suture to
close the anterior hiatus if there is concern that the posterior closure is bringing the esophagus so far anterior that it may be creating an angle as the esophagus exits the chest.
BOX 2 Equipment for Laparoscopic Antireflux
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Surgery
Basic Laparoscopic Supplies
0- and 30-degree laparoscope, camera, and video equipment 5- and 12-mm ports Veress needle Suction-irrigation device
Laparoscopic Energy Devices
Hook electrocautery Bipolar or ultrasonic vessel-sealing device
Specialized Equipment
Liver retractor (e.g., Nathanson) 52-Fr Bougie (optional for partial fundoplication) Laparoscopic suturing supplies ½-inch Penrose drain Equipment for upper endoscopy
FIG. 3 Port placement for laparoscopic antireflux surgery. The camera
port is positioned approximately 15 cm below the left costal margin, 2 cm to the left of midline. The Nathanson liver retractor is inserted through a stab incision in the epigastrium to the left of midline.
Steps of the Procedure: Creating a 360-Degree Nissen Fundoplication
As previously discussed, we prefer to perform a complete fundopli­cation in patients with normal esophageal motility. We believe this provides a more durable repair, and we find that the geometry of a complete fundoplication lends itself to greater reproducibility from a technical standpoint.
1. Orientation of the wrap a. The fundus and greater curve of the stomach is retracted
medially, and a marking stitch is placed on the posterior
ESOPHAGUS
FIG. 4 Completion of the circumferential crural dissection. This illustration
depicts the view immediately before insertion of the Penrose drain.
(From Yates RB, Oelschlager BK, Pelligrini CA. Gastroesophageal reflux disease and hiatal hernia. In: Townsend etal., eds. Sabiston Textbook of Surgery. 20th ed. Philadelphia: Elsevier; 2017:1043–1064.)
11
fundus approximately 3 cm below the angle of His and 2 cm inside the greater curve.
b. The posterior fundus is passed behind the esophagus, and the
point on the stomach where the marking stitch was placed is lifted anteriorly against the right side of the esophagus.
c. A point on the anterior fundus is identified that mirrors the
location where the marking stitch was placed posteriorly (approximately 3 cm away from the angle of His and 2 cm from the greater curvature of the stomach). This point on the stomach is pulled up along the left side of the esophagus.
d. A “shoe-shine” maneuver is performed to assess the symme-
try of the fundoplication before bringing the two sides of the fundus together anterior to the esophagus (Fig. 5). With this construction, the greater curve of the fundus should run lon­gitudinally posterior and to the left of the esophagus (and thus is no longer visible when suturing the fundoplication).
2. Suturing the fundoplication a. The first stitch is placed, bringing the anterior and posterior
fundus together at the points identified in the previous steps. The marking stitch and Penrose drain are then removed. A 52F bougie is then passed down the esophagus and into the stomach.
b. The remaining two or three sutures are placed with the bougie
in place to complete the fundoplication. The bougie is then removed (see Fig. 5).
c. We place a coronal suture on each side of the wrap that incor-
porates the top of the fundus/wrap, a partial thickness bite of the esophagus, and the ipsilateral crus. This helps fix the orientation of the fundoplication in the abdomen (see Figs. 2A and 5).
d. We also typically place a suture between the posterior aspect
of the fundoplication and where it naturally rests against the crural closure as an additional fixation point.
e. We perform routine upper endoscopy upon completion of
the fundoplication to evaluate and document the appropriate appearance of the newly augmented flap valve.
Steps of the Procedure: Creating a 270-Degree Posterior Toupet Fundoplication
In patients with manometric evidence of ineffective esophageal motility, we typically recommend a partial fundoplication. When
12 SURGICAL MANAGEMENT OF GASTROESOPHAGEAL REFLUX DISEASE
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2. Completing left side of the fundoplication a. The anterior fundus is pulled laterally to remove the redun-
dant stomach from behind the esophagus.
b. A left coronal suture is placed, incorporating the anterior fun-
dus, a partial bite of the esophagus, and the left crus (again, just like the Nissen orientation).
c. Two additional sutures are placed between the esophagus (to
the left of the anterior vagus nerve) and posterior fundus, completing the left side of the fundoplication (see Fig. 2C).
d. We routinely perform an upper endoscopy upon completion
of the fundoplication to evaluate and document the appropri­ate appearance of the newly augmented flap valve.
POSTOPERATIVE CARE, SURGICAL COMPLICATIONS, AND OUTCOMES
Postoperatively, acid suppression therapy is routinely discontinued, and all medications are administered in either crushed or liquid form for 4 weeks. We typically admit patients to the hospital on a liquid diet and monitor for appropriate pain control and PO intake before discharge the following day. Although some surgeons routinely obtain a barium esophagram on the first postoperative day, we have not adopted this practice. Instead, patients who are able to tolerate a liquid diet without issue are advanced to a soft esophageal diet upon discharge on the first postoperative day, and this diet is maintained
52-French bougie
FIG. 5 Creating a 360-degree Nissen fundoplication. The “shoe-shine”
maneuver is performed by grasping the posterior and anterior fundus with the left and right hand, respectively, 3 cm from the angle of His, and 2 cm from the greater curvature of the stomach. (From Oelschlager BK, Eubanks
TR, Pellegrini CA. Hiatal hernias and gastroesophageal reflux disease. In: Townsend CM, Beauchamp RD, Evers MB, etal., eds. Sabiston Textbook of Surgery. 19th ed. Philadelphia: Elsevier; 2012.)
considering the geometry of a 270-degree (Toupet) fundoplication, the inner circumference of the fundoplication should approxi­mate that of the esophagus, while the outer circumference should be appropriately redundant, resembling a crescent with rounded corners in cross-section. This geometry provides volume to the fundoplication, which supports the intended flap-valve effect. The constructed geometry should be very similar to that of a Nissen, just without bringing the stomach together, thus the following descrip­tion is very similar. Of note, we do not routinely use an esophageal bougie when performing a partial fundoplication.
1. Orienting and creating the right half of the wrap. a. The fundus and greater curve of the stomach is retracted
medially, and a marking stitch is placed on the posterior fundus approximately 3 cm below the angle of His and 2 cm inside the greater curve.
b. The posterior fundus is passed behind the esophagus, and the
point on the stomach where the marking stitch was placed is lifted anteriorly against the right side of the esophagus.
c. A coronal suture is placed on the right side, incorporating the
posterior fundus, a partial thickness bite of the esophagus, and the right crus (just like in a Nissen).
d. A posterior stitch is placed to fixate the wrap to where it nat-
urally lies against the crural closure.
e. Two additional sutures are placed between the esophagus (to
the right of the anterior vagus nerve) and posterior fundus, completing the right side of the fundoplication (see Fig. 2C).
for 4 weeks.
Mild dysphagia is very common following ARS, and patients should be counseled to expect this during their preoperative and postoperative diet education. Similarly, patients are typically unable to belch or vomit following ARS, and many patients may experience mild bloating discomfort, abdominal distention, or epigastric pain. For most patients, both dysphagia and gas bloat should improve after 6 to 8 weeks. If these symptoms persist beyond this timeframe, endoscopic dilation of the wrap may be considered.
Long-term outcomes associated with laparoscopic ARS can be measured by examining patient-reported symptoms, objective measures of distal esophageal acid exposure, resumption of PPI use, complications of GERD, or rates of reoperation. Thus, depending on the primary outcome examined, definitions of success and failure vary across studies. In general, available studies demonstrate a 15% to 30% recurrence rate for GERD at 10 years in patients following laparoscopic ARS. Most patients with recurrent GERD are medically managed with acid suppression therapy, while a minority (less than 5%–10%) undergo reoperation. As mentioned previously, ARS is associated with higher complication rates compared with acid sup­pression therapy. In studies that focus on patient-reported outcomes, ARS generally outperforms medical therapy when patients are surveyed on GERD-related symptoms and quality of life. Patient-re­ported satisfaction following ARS consistently approaches 90% or higher.
SPECIAL CONSIDERATIONS
It is important to distinguish ARS from paraesophageal hernia repairs as the surgical evaluation and approach to GERD differs from that of paraesophageal hernias. This can be confusing because fundoplications are often performed in conjunction with paraesoph­ageal hernia repairs, thus the anatomic result following completion of both procedures is essentially identical. However, in the absence of a paraesophageal hernia, adequate circumferential mobilization of the distal esophagus should almost always provide enough intraab­dominal length to obviate the need for an esophageal lengthening procedure. When performing ARS in patients with a small- to moderate-sized sliding hiatal hernia, the lower esophageal sphincter should (by definition) reach the intraabdominal cavity. Thus, we reserve the discussion of Collis gastroplasty and esophageal length­ening procedures for chapters focused on paraesophageal hernia repair. In the same vein, although the use of absorbable mesh has
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been studied and debated in the context of paraesophageal hernia repairs, there is no real indication for mesh use in laparoscopic ARS for GERD.
In patients who develop recurrent GERD symptoms following ARS, it is important to review the prior operative records and obtain a complete workup as described earlier in this chapter. Herniation of the wrap cephalad into the mediastinum is the most common cause of anatomic failure in patients with a previous fundoplication (Fig. 6). Failure can also result from an inappropriately constructed fundoplication that incorporates the body of the stomach (Fig. 7) or simply from loosening of the wrap over time. Anatomic failures can lead to recurrent GERD and new symptoms of dysphagia, odynopha­gia, or epigastric pain. Just as in the initial management of GERD, patients presenting with typical reflux symptoms following ARS can often be managed medically. In patients with persistent dysphagia, epigastric pain, or poorly controlled reflux symptoms despite med­ical therapy, surgical revision may be considered after careful eval­uation to identify anatomic causes of failure while ruling out other possible etiologies. In general, caution should be exercised when considering a surgical revision as the complication rates associated with revisional surgery are higher than for first-time ARS.
FIG. 6 Upper gastrointestinal barium esophagram depicting
herniated fundoplication. Original radiographs (top). Herniated position of fundoplication is outlined in black (bottom). Yellow arrowheads depict diaphragmatic impression.
When approaching a revisional operation, the surgeon should always plan to take down the prior fundoplication as this is the only way to evaluate the construction of the prior wrap and ensure the correct construction of a new fundoplication. After both halves of the fundoplication have been dissected free, the right half should be passed behind the esophagus to restore the normal orientation of the stomach and confirm that the wrap has been completely taken down before creating a new fundoplication. Importantly, we have encountered many barium esophagrams with radiology reports suggesting complete dehiscence of a previous fundoplication. In our institution’s collective experience performing revisions, we have never encountered a complete dehiscence in the operating room. There is always a wrap that needs to be properly identified and taken down. Finally, when evaluating patients who have failed two prior antireflux procedures, we generally do not consider a third attempt to redo the wrap. If indications arise to consider another revision after multiple prior failures, a revision may be considered, but the surgeon and patient should be prepared for the possibility of a partial gastrec­tomy and Roux-en-Y reconstruction with either a gastrojejunostomy or potentially an esophagojejunostomy. This is, of course, is a major operation, and the associated risks and lifelong dietary modifications
14 NEW APPROACHES TO GASTROESOPHAGEAL REFLUX DISEASE (LINX)
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should be weighed against the severity of the patient’s symptoms when counseling patients who have failed multiple attempts at ARS.
S u g g e S t e d R e a d i n g S
B
A
A
Correct
Incorrect
B
B
A
A
B
Gunter RL, Shada AL, Funk LM, Wang X, Greenberg JA, Lidor AO. Long-
Term quality of life outcomes following Nissen versus Toupet fundoplica­tion in patients with gastroesophageal reflux disease. J Laparoendosc Adv Surg Tech A. 2017;27(9):931–936.
Håkanson BS, Lundell L, Bylund A, Thorell A. Comparison of laparoscopic
270° posterior partial fundoplication vs total fundoplication for the treatment of gastroesophageal reflux disease: a randomized clinical trial. JAMA Surg. 2019;154(6):479–486.
Lødrup A, Pottegård A, Hallas J, etal. Use of proton pump inhibitors after
antireflux surgery: a nationwide register-based follow-up study. Gut. 2014;63:1544–1549.
Morrow E, Bushyhead D, Wassenaar E, Hinojosa M, Loviscek M, Pellegrini C,
Oelschlager B. The impact of laparoscopic anti-reflux surgery in patients with Barrett’s esophagus. Surg Endosc. 2014;28(12):3279–3284.
Raghu G, Pellegrini CA, Yow E, etal. Laparoscopic anti-reflux surgery for the
treatment of idiopathic pulmonary fibrosis (WRAP-IPF): a multicentre, randomised, controlled phase 2 trial. Lancet Respir Med. 2018;6(9):707–
714.
FIG. 7 A wrap can be incorrectly constructed by suturing the fundus to
the body of the stomach. (From Smith CD, McClusky DA, Rajad MA, Lederman AB, Hunter JG. When fundoplication fails: redo? Ann Surg. 2005;241[6]:861–869.)
New Approaches to Gastroesophageal Reflux Disease (LINX)
Tom R. DeMeester, MD
etween the early 1960s and early 1970s, Drs. Rudolf Nissen, Ronald Belsey, and Lucius Hill introduced the golden era of
B
antireflux surgery. These physicians designed procedures that took down a hiatal hernia, altered the anatomy of the gastroesophageal junction with a fundoplication of various degrees, and stopped reflux of gastric juice into the esophagus. In 1975, the first randomized controlled study confirmed the superiority of surgical over medical therapy with antacids. Surgery was off and running.
All came to a dramatic halt when the Nobel Prize was awarded to Sir James W. Black in 1988. He discovered an approach to drug development called rational drug design structure. Simply stated, if the pathophysiology of a disease is properly understood, a specific drug could be synthesized to interrupt key points in the pathogenesis and cure the disease. He used this concept to discover the beta and H cimetidine. Cimetidine became the first drug ever to exceed $1 billion per year in sales. The methodology eventually led to the development of proton pump inhibitors (PPIs), which block the secretion of acid by the parietal cells. The aim of these drugs is to increase the pH of the gastric juice, which, along with the lower esophageal sphincter, contribute to gastroesophageal reflux
receptor antagonists, propranolol and
2
disease (GERD). By the 1980s, the clinical benefits of PPIs were demonstrated dramatically by the abolishment of GERD symp­toms and the virtual elimination of acid-induced reflux esopha­gitis, strictures, and giant Barrett’s ulcers. Now medicine was off and running.
WHY A NEW SURGICAL ANTIREFLUX
PROCEDURE?
After 35 years of experience with more than 20 million GERD patients on prescribed PPIs, physicians have developed some concerns. Despite the introduction and use of the new powerful acid-suppression drugs over this period, the incidence of GERD continues to increase by 30% every 10 years, and 30% to 40% of patients on PPI therapy have only partial relief of their symptoms. Between 2% and 3.5% of the 20 million patients with GERD receiv­ing PPI therapy develop Barrett’s esophagus every year, of which
0.5% to 1% progress to esophageal adenocarcinoma. Despite this high percentage of patients with a partial response and disease pro­gression on PPI therapy, less than 1% seek surgical therapy. These concerns have given rise to the thought that the time has come for a change in the treatment strategy of GERD. The current treatment strategy focuses only on one of the two determinants of the disease, the acid composition of the gastric juice, whereas the other deter­minant, failure of the lower esophageal sphincter (LES), is ignored. This focus on PPIs and disregard for the LES is likely the result of a historical misunderstanding that GERD is primarily an acid peptic disease. The primary abnormality in GERD is the loss of an effec­tive LES to keep the gastric juice in the stomach. This was pointed out in 2003 in a publication by Dr. G. Wetscher and colleagues
from Innsbruck, Austria. They showed that the recurrence of reflux
Distension or dilation
Effacement of the LES
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symptoms and/or endoscopic esophagitis in patients on PPIs was related to the functional status of the LES and esophageal body. Patients with both a defective LES and esophageal contractions had an 80% recurrence rate compared with 39% in those patients with a defective LES and normal esophageal body contractions, or 8% in those with both a normal LES and normal esophageal contrac­tions. They concluded that the status of the LES is a critical factor in the effectiveness of PPI therapy. The medication works well in patients with a normal LES and not so well in patients who have a defective LES. In the latter situation, reflux episodes continue at the same frequency whether the patient is off or on the medication. The only difference is a change in the pH of the refluxed gastric juice. As a consequence, 85% of patients on PPIs still experience GERD-related symptoms, and in 35% the symptoms have reached the level to cause dissatisfaction with PPI therapy. In an effort to improve symptom control, the prescriptions for double-dose PPIs have increased by 50% in the past 7 years, and 42% of patients sup­plement their prescription with other acid-suppression medication in an effort to gain relief. Of greatest concern is that 10% to 15% of patients have disease progression while on PPI therapy, and the longer the disease persists, the greater the number of patients who progress.
Over the past 35 years, antireflux surgery has not fared much better. Even though the surgery can be performed through a lapa­roscope and achieve effective control of reflux symptoms and heal esophagitis, the outcomes vary in their effectiveness and durability, and the early surgical revision rate is too high. The procedures have significant side effects in that patients are unable to belch or vomit, risk having increased flatulence and postprandial bloating, and have a small possibility of bothersome dysphagia. When performed by the occasional surgeon, only 61% of patients are completely satisfied with their operation. These results discourage patients against anti­reflux surgery, and at present less than 1% of GERD patients have surgical therapy. Unless there are some fundamental improvements in surgical therapy, it appears that the use of surgery for the treatment of GERD will reach a standstill.
NEW SURGICAL APPROACH TO GERD
The ideal surgical procedure to improve the function of the LES in a patient with GERD would be a minimally invasive, short, outpatient procedure that augments the LES function without causing anatomic alterations. Based on the effectiveness of the Nissen fundoplication, it should have a greater than 80% probability of normalizing esoph­ageal acid exposure and a 90% probability of eliminating GERD-re­lated symptoms. It should allow an unrestricted diet and cause no long-term side effects such as persistent dysphagia, symptomatic bloating, increased flatus, or the inability to belch or vomit. Further, it must be reversible without sequelae.
Over the past 10 years, studies on the pathophysiology of the LES have opened the door for technology to design a new device that meets the ideal requirement for a new surgical procedure for the treatment of GERD. These studies have shown that gastric distension or dilation after meals can cause effacement of the LES, resulting in progressive shortening of its length and, as a consequence, loss of its competency (Fig. 1). This process exposes the effaced squamous mucosa of the distal esophagus and the underlying muscle of the LES to gastric juice. The inflammatory injury that occurs destroys the squamous mucosa, heals by the induction of metaplastic cardiac mucosa, and induces permanent damage to the muscle of the LES, resulting in a loss of its abdominal length, overall length, and pres­sure. The resulting structurally defective LES allows repetitive LES effacement to occur with ease, resulting in escalation of the degrees of esophageal exposure to acidic bile containing gastric juice. Placing a loose ligature or ring around the inferior border of the LES can stop the effacement and has formed the basis for the design of new devices to augment LES function.
ESOPHAGUS
FIG. 1 Effacement and shortening of the length of the lower esoph-
ageal sphincter (LES) that occurs with gastric distension or dilation after meals and, as a consequence, loss of its competency. The process exposes the effaced squamous mucosa of the distal esophagus (red line) and the underlying muscle of the LES (black area below the red line) to gastric juice.
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LINX ANTIREFLUX DEVICE
One of the new devices is the LINX Reflux Management System (Torax Medical, St. Paul, MN). It is a simple procedure, performed laparoscopically, that does not alter gastric or gastroesophageal junc­tional anatomy, augments the LES as a functional barrier to reflux, and can be reversed easily if necessary, thereby preserving the option for fundoplication or other therapies in the future. The LINX pro­cedure is designed to limit technical variability, which will result in more standardization of antireflux surgery and more consistent clin­ical outcomes. The LINX device consists of a series of titanium beads with magnetic cores hermetically sealed inside (Fig. 2). The beads are interlinked with independent titanium wires to form a dynamic ring designed to conform to the changing physiologic movements of the esophagus during swallowing. The device was designed to use the magnetic attraction between adjacent beads to prevent the opening of the LES by distal to proximal effacement and shortening of its length caused by episodes of gastric distension or postprandial gastric dilation secondary to adaptive relaxation. The device is sized to fit around the external circumference of the esophagus at the distal end of the LES without compressing the esophageal muscula­ture. The beads separate to allow the transport of a food bolus into the stomach, to relieve gastric distension by belching or nausea by vomiting (Fig. 3).
The LINX device was not designed to deter reflux episodes caused by pressure challenges that affect the whole abdominal envi­ronment. To deter these challenges requires sufficient esophageal length in the abdominal domain to allow the LES to be compressed by changes in the abdominal environmental pressure that occur with daily living and working. For this reason, it is recommended that, if possible, the LINX device be implanted with minimal disruption of the phrenoesophageal ligament to preserve sufficient length of esophagus in the abdominal domain.
LINX IMPLANTATION PROCEDURE
The LINX magnetic sphincter augmentation device is implanted laparoscopically under general anesthesia. Surgical ports are placed similar to the pattern used for the laparoscopic Nissen fundoplica­tion with one exception. The dissection port in the patient’s right upper quadrant is placed far laterally to optimize the visualization and sizing of the esophagus at the gastroesophageal junction. A lim­ited focus dissection is ideal for implantation of the LINX device in a patient without a hiatal hernia. When performing a limited focus
16 NEW APPROACHES TO GASTROESOPHAGEAL REFLUX DISEASE (LINX)
Closed Open
AB
tanium
LINX device
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Ti
wires
Roman
arch
Magnetic
core
FIG. 2 Engineering schematic of the magnetic sphincter augmentation device. The device consists of an expansible bracelet of magnetic beads designed to
be placed surgically around the exterior surface of the distal end of the lower esophageal sphincter (LES). Each bead is composed of a titanium case con- taining a magnetic core of small disk-shaped magnets. The beads are connected by titanium wires of specific lengths that limit the distance any two individual beads can move apart. When the device is closed (A), the magnetic force is sufficient to prevent effacement and opening of the LES yet is weak enough to allow the device to open (B) with esophageal peristalsis. When the device is closed, the Roman arch construction prevents compression of the esophageal tissues.
Titanium
case
Diaphragm
Esophagus
LES
Stomach
A
FIG. 3 The LINX magnetic sphincter augmentation device is implanted around the inferior border of the lower esophageal sphincter (LES), as shown.
(A) The magnetic device is shown in the closed position, which prevents effacement and opening of the LES and subsequent reflux. Each magnetic bead
rests on the adjacent beads to prevent compression of the esophageal tissues. (B) The device is shown in the open position, which allows transport of food by esophageal peristalsis, belching of an overdistended stomach, and vomiting when necessary.
dissection, the surgeon must preserve and not dissect the phren­oesophageal ligament.
The surgical dissection begins by mobilizing the posterior gastric fundic wall off the lateral surface of the left crus to expose the caudal anterior edge of the left crus. In doing so, as few short gastric vessels as possible are divided. A 1-cm segment along the anterior margin of the left crus just above the crural decussation is identified. At this location, a medial dissection is performed just beneath the esophagus to form a pocket target for the right-sided tunnel dissection. In per­forming this dissection, care is taken not to enter the mediastinum. After the pocket target is made, the dissection is switched to the right side of the esophagus. The gastrohepatic ligament is opened by making two windows, a small one just superior to the hepatic branch of the anterior vagal nerve and a larger one inferior to the hepatic branch. The inferior window allows access to construct a retroesoph­ageal tunnel through a 1- to 2-cm incision in the peritoneum along the anterior edge of the right crus just above the crural decussation. Using a dissector placed through the far lateral right upper quadrant port and the inferior window in the gastrohepatic ligament, a gentle dissection is made toward the left crus just to identify the posterior
Bolus
LINX device
B
vagal nerve as it leaves the esophagus and drops posterior to the celiac plexus (Fig. 4A). Bleeding from the small vessels can obscure the dissection and is controlled with judicial use of cautery. Delicately, a tunnel is dissected in a right-to-left direction, between the posterior vagal nerve and the posterior esophageal wall, to connect with the previously constructed pocket target on the anterior margin of the left crus. Entering the mediastinum during the tunnel dissection should be avoided. The dissector is passed through the pocket target and into the left upper quadrant. The dissector is removed from the left upper quadrant, drawing a ¼-inch Penrose drain through the tunnel and securing its right and left ends for retraction. In line with the expected position of the device, the fibroareolar tissue from the right and left lateral esophageal surfaces is removed, and a trench is constructed through existing fat on the anterior surface of the esophagus below the inferior leaf of the phrenoesophageal ligament. The circumference of the esophagus then is measured to choose the proper size of the LINX device to be implanted. The sizing tool is a laparoscopic instrument with a soft, circular curved tip that is actuated by coaxial tubes through a handset. The handset contains a numerical indicator that corresponds to the size range of the LINX