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Spastic Motility Disorders
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Primary esophageal motility disorders (PEMDs) encompass both spastic disorders and achalasia. Spastic disorders include nutcracker esophagus, diffuse esophageal spasm (DES), and hypertensive lower esophageal sphincter (HLES). These rare disorders can present with variable or nonspecific symptoms and can be difficult to diagnose and treat. Symptoms frequently include chest pain, GERD, regurgitation, and less commonly dysphagia. The clinician must pay careful attention to presenting complaints and beware of what symptoms typically respond to treatments and which do not. It is important to distinguish between the primary motility disorders just mentioned and those symptoms secondary to GERD. GERD is a significant cause of esophageal dysmotility and should be evaluated for its presence. Its successful treatment, medically or surgically, often mitigates the symptoms suffered by many patients. These patients may be initially diagnosed with esophageal motility disorders but in actuality have a significant reflux component to their problem.24–27 Secondary causes of esophageal motility disorders can include diabetes mellitus, Chagas' disease, collagen vascular diseases, and multiple sclerosis. If such conditions exist, their severity and prognosis should be taken into consideration when forming a diagnosis and prior to embarking on any therapy.
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Patient Presentation and Evaluation
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Prior to investigation of the esophagus as the cause of symptoms, a cardiopulmonary evaluation should be performed to rule out the heart or lungs as the cause. The evaluation of motility disorders should include a careful history taking. This may help clarify the diagnosis and should allow the examiner to pick up on any confounding psychiatric illness or disorder that may be responsible, such as rumination syndrome. A systematic workup should include endoscopy and UGI barium swallow to evaluate the anatomy and rule out malignancy or other lesions as a cause. Esophageal manometry is an essential component of the workup, and 24-hour pH study should be performed to evaluate for reflux (Fig. 14-10).
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Diffuse Esophageal Spasm
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Diffuse esophageal spasm (DES) was first described by Osgood in 1889.28 Typically, patients affected by DES will complain of chest pain and dysphagia, and may present with functional obstructive symptoms. Symptoms of DES can be difficult to distinguish from GERD; both pH and manometry should be performed as part of the workup to evaluate the patient. If abnormal reflux is found on testing, the first treatment strategy should be to control GERD with antisecretory therapy. The defining characteristics of DES on manometry include greater than 10% (but <100%) of wet swallows that are followed by simultaneous esophageal contractions of amplitude 30 mm Hg or greater (Fig. 14-11).29,30 LES dysfunction, manifested by improper relaxation and/or hypertensive state, is seen in over half of patients diagnosed with DES.31 Intermittent peristalsis and prolonged contractions are also findings seen on manometry. DES is a rare true finding and is estimated to be found only in 3–5% of patients evaluated for an esophageal motility disorder.32 Whereas previously there was thought to be little role for surgical treatment in DES, more recent reports of small series have shown good results for relief of dysphagia after esophageal myotomy in up to 80% of highly selected patients, while chest pain is more difficult to cure.24,31,33 A careful, thorough workup and exclusion of GERD as a confounding factor should be done before attempting to diagnose and surgically treat DES. Medical management is an appropriate initial approach.
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Nutcracker esophagus (NE) was first described by Brand and associates34 in 1977 and named as such by Castell several years later.35 Typical presenting symptoms of patients with NE include chest pain and less frequently dysphagia. Its defining characteristics on manometry include hypertensive esophageal contractions of greater than 180 mm Hg (Fig. 14-12). Patti and colleagues performed myotomy for these patients and observed that dysphagia was controlled in 80% of patients, but that chest pain persisted in 50% of them.31 Interestingly, in the patients with recurrent pain, they developed dysphagia postoperatively, possibly because of weakening of peristalsis by performing the myotomy. Most patients with this manometric finding consistent with NE and presenting with chest pain do not need an operation, and consideration for surgery should rather be carefully given to patients with dysphagia as the presenting symptom. The best candidates may be a small subgroup in which manometry demonstrates a hypertensive LES in addition to NE findings as well as a functional obstruction on UGI. As with DES, one must evaluate for GERD and treat if present. GERD, when present in conjunction with hypertensive esophageal contractions, can be an inciting factor causing further esophageal irritation in a hypersensitive esophagus. Therapy aimed at correcting abnormal acid exposure and irritation can lead to significant improvement in symptoms. The mainstay of treatment is medical therapy. Calcium channel blockers have shown benefit in symptom improvement.36 Tricyclic antidepressants may also provide symptom relief and benefit to patients.
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Hypertensive Lower Esophageal Sphincter
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Hypertensive lower esophageal sphincter (HLES) is a condition defined as having a resting LES pressure of greater than 45 mm Hg with intact, normal peristalsis (Fig. 14-13). Incomplete relaxation of the LES may also be a feature. The condition was first described in 1960.37 Patients with HLES can be a heterogeneous group and can present with symptoms of chest pain and/or dysphagia. They may also have symptoms of a functional obstruction at the LES. Presentation can be with isolated symptoms or in association with GERD. Careful history taking and a thorough workup with manometry and pH testing are essential to clearly define the symptoms and the primary problem in terms of esophageal function. Therapy should be tailored to the presenting symptoms. Medical management to reduce LES pressures with calcium channel blockers, botulinum toxin, and phosphodiesterase inhibitors is typically the first-line approach in management. These drugs can have significant side effects and decreasing efficacy with time. In patients with GERD and manometric findings of HLES, Nissen fundoplication has shown good results in improvement of dysphagia and chest pain.38,39 This suggests that reflux disease may be the etiology in these patients. Patients with dysphagia or chest pain as their predominant symptom and workup findings of only isolated HLES without GERD are more likely to benefit from myotomy and partial fundoplication for symptom relief, suggesting a primary sphincter dysfunction as the etiology of their symptoms. Good results have been reported by several groups that have used myotomy and partial fundoplication to treat this subset of patients, with relief of symptoms persisting as far as 3 years out.31,38,40 While medical management is usually a reasonable first-line, conservative approach to treatment of HLES, in carefully selected and thoroughly worked up patients surgical treatment with either Nissen fundoplication or myotomy and partial fundoplication (depending on manometric and pH test findings) can produce good results. As HLES is a rare disease with heterogeneous presentation, the importance of carefully and thoroughly working up affected patients before embarking on therapy cannot be overemphasized.
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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 significantly 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 first line of therapy. Surgery may be offered to carefully selected patients in whom an operation can address a discrete etiology such as abnormal GERD or isolated LES dysfunction.
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Idiopathic achalasia is a primary motor disorder affecting the esophagus. Achalasia, which is typified 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 Western world.41 It is, however, of all the previously mentioned motility disorders, the most common PEMD. The histopathologic hallmark of the disease remains near complete or total loss of the myenteric plexus ganglion cells as a result of injury and fibrosis 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 inflammatory infiltrate.42–44 The inciting event or trigger may relate to cytotoxic T-cell activation by latent herpes simplex virus 1 (HSV-1) antigen exposure.45,46 In addition, nitric oxide (NO) synthesis, a mediator of LES relaxation, is often impaired in the face of preserved cholinergic neuronal function.47–49 These two insults result in loss of peristalsis and impaired relaxation of the LES, which in turn lead to the pathophysiologic findings of impaired esophageal emptying, aperistalsis, and a nonrelaxing LES.
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Achalasia can occur in patients of all ages but typically presents in patients in the second to fifth 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 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. These 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 effect acting like a stomach reservoir, one finds 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 (<6 months) and significant 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.
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Patients should be worked up in a systematic, methodical fashion. The workup has several components. An upper GI esophagram should first be performed to assess the anatomy. This 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 findings on barium esophagram include distal tapering to the GE junction, resulting in a “bird's beak” appearance. Air fluid 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.
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Manometry is used to confirm the diagnosis of achalasia. Aperistalsis of the esophageal body and impaired relaxation of the LES are the hallmark findings on manometry, with aperistalsis being a requisite finding. 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.
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Endoscopy is an essential part of the workup for achalasia patients. This offers 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.
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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.
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Therapy 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 esophageal emptying by relaxing or disrupting the muscle fibers of the LES.
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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 effectiveness and inconsistent absorption, their use is limited. Impaired esophageal emptying can affect their ingestion and absorption. In randomized controlled trials, calcium channel blockers have not shown significant success in improving clinical symptoms, despite lowering LES pressures.50,51 Sildenafil, a phosphodiesterase inhibitor, has been shown to have potent relaxing effects on the LES,52 but its clinical use is limited by poor tolerance and side effects. Nitrates, which can be used in sublingual formulation to overcome poor absorption, tend to work better than calcium channel blockers for symptom relief.53 Their use, however, can lead to undesired side effects such as hypotension and headache and, like all medical therapies, their efficacy decreases with time. Pharmacologic therapy should be pursued only in patients who, for medical reasons, are unable to undergo other therapies.
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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. This steadily declined over time to 40.6% at 12 months, with 46.6% of patients requiring repeat injection.54 While botulinum toxin injection therapy may offer temporary relief of symptoms, its effects 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 87% in the surgical arm remained symptom free.55 Multiple injections can further complicate future surgical therapy due to the submucosal fibrosis that can result, making myotomy more difficult and increasing the risk of perforation.56 Endoscopic botulinum toxin injection may offer an alternative to those unwilling or unable to undergo more invasive procedures but has a limited role in the treatment of the disease.
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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. Different types of dilations have been used in the past, including fixed diameter dilators, mercury-weighted balloons, and water-filled balloons. The most controlled and consistent results are seen with the use of noncompliant pneumatic balloon dilators, such as the Rigiflex balloon dilator (Boston Scientific, Boston, MA).57 Campos et al, in their meta-analysis, evaluated 15 studies involving 1065 patients 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 efficacy than botulinum toxin injection but still shows significant 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 This risk increases with the presence of significant esophageal dilation, hiatal hernia, and epiphrenic diverticula (ED). These should be considered relative contraindications to pneumatic dilation. Between the endoscopic therapies mentioned, pneumatic balloon dilation is a more efficacious procedure but has greater risk of perforation compared to botulinum toxin injection.
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Surgical myotomy was first described by Ernst Heller in 1913.58 His original description involved performing both an anterior and posterior myotomy. This has evolved in most centers to performing an anterior myotomy only. Esophageal myotomy for achalasia is associated with good long-term 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 approximately 3 years postprocedure.41,54,59 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. These approaches eventually evolved to the minimally invasive approaches via thoracoscopy or laparoscopy. Shimi et al reported the first laparoscopic Heller myotomy in 1991, while Pellegrini et al reported the first thoracoscopic approach in 1992.60,61 Drawbacks to this thoracoscopic approach included the need for single-lung ventilation, postoperative chest tubes, and being unable to perform an antireflux procedure. The minimally invasive approach has moved predominantly to the laparoscopic myotomy approach that has eliminated these drawbacks of the thoracoscopic approach. Laparoscopy offers 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 antireflux 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 reflux symptoms when combined with a partial fundoplication (14.9 vs 28.3%).54
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The two main debates surrounding surgical myotomy have centered on whether or not to include an antireflux 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 antireflux procedure to a standard Heller myotomy has been thought to reduce these symptoms and improve outcomes.
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This issue has been studied in a prospective, randomized trial by Richards et al, comparing Heller myotomy with Heller myotomy plus Dor (anterior) fundoplication. They demonstrated that the pathologic occurrence of GER, as defined 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 fundoplication.62 Some surgeons have advocated in the past for inclusion of a floppy 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 floppy-Nissen fundoplication. At 60 months of follow-up, no statistically significant difference in GER symptoms between the two groups were seen; the rate of dysphagia, however, was found to be significantly higher in the floppy-Nissen fundoplication group when compared to the Dor fundoplication group (15 vs 2.8%). They concluded that both antireflux procedures offered adequate protection from GER, but that recurrence of dysphagia was significantly higher when Nissen fundoplication was performed.63 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 antireflux 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.
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The 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. This 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. This length was chosen with the intent of being long enough to relieve the functional obstruction to the esophagus, while in an effort to preserve an antireflux barrier.64 The 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 fibers. 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 17%).65 We continued to follow and then compared a cohort of 52 of these patients at a median follow-up of 46 months. No significant differences 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) versus 18% of SM/Dor patients (10% required endoscopic treatment, 8% required reoperation).66 We feel that the Toupet is a better antireflux operation in combination with extended myotomy. Reasons for its superior efficacy 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 fibers and symptom recurrence. Our study compared two different 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 antireflux procedure. We feel that extended myotomy of 3 cm below the GE junction should be a routine practice when performing a Heller myotomy.
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Laparoscopic Heller Myotomy.
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The 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. This is especially important during the creation of a myotomy. In contrast, we use 5-mm, 30-degree laparoscopes for PEH repairs and first-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.
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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 significantly dissect the posterior attachments of the esophagus, except to provide enough intra-abdominal esophagus to perform a good fundoplication. The 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. This 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. The anterior GEJ fat pad to the left of the anterior vagus nerve is resected. This allows for accurate identification of the GEJ at the time of myotomy.
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At this time, a 50F lighted bougie is passed into the body of the stomach. The transillumination provided aids in identification of the submucosal plane. A laparoscopic Babcock clamp, first applied partially opened over the bougie, is used to gently drag the tissue over and around the bougie to provide tension and exposure. The 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 fibers apart, exposing the submucosa. Entering the correct plane takes patience and careful dissection. The submucosa of the stomach contains a rich plexus of vessels that can be used as a visual identifier. Once the appropriate plane is identified, the myotomy is carried cephalad. Only minimal electrocautery is used during performance of the myotomy (Fig. 14-17).
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The correct plane may be difficult to identify on the stomach, as the sling fibers 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 fibers of the esophagus. We first divide the outer longitudinal muscle fibers and then the inner circular layer. The myotomy is carefully extended and taken above the level of the anterior vagus nerve as it crosses from left to right over the esophagus. The extent of the myotomy is to take it as proximally as is safe. Typically, one can get 6–8 cm above the GE junction. The 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 fibers on tension, with the surgeon's left hand holding the right-sided fibers. In this fashion, the myotomy is completed.
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Bleeding from submucosal vessels that are mistaken for muscle fibers 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 coming forth. Intraoperative endoscopy can be used to confirm 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.
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Intraoperative endoscopy is carefully performed to evaluate for the completeness of myotomy and to evaluate for injury. If all muscle fibers have been correctly divided, an open GE junction will clearly be visible on endoscopy, without indentations from undivided fibers. In addition, with gentle insufflation, injury to the mucosa can be seen both endoscopically and laparoscopically.
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A Toupet (posterior) fundoplication is performed for the antireflux procedure as the final part of the operation. A suture is placed on the posterior portion of the fundus, 3 cm below the GE junction and 2 cm away from the line of the divided short gastric vessels. This is used as a reference point to ensure a symmetric posterior wrap. The fundus is brought posteriorly behind the GE junction, and the reference suture is grasped and brought up to the edge of the myotomy. The fundus is sutured to the right crus to alleviate tension, using 2-0 silk suture. The 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). After completing the wrap, the ports and liver retractor are removed and the port sites are closed, concluding the case.
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A Dor fundoplication is an acceptable antireflux procedure and is technically easier to perform than the Toupet, as it requires less dissection, especially of the posterior stomach (Fig. 14-20). The Toupet does a better job of stenting open the divided muscle fibers 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 antireflux portion of the procedure because of the high incidence of postoperative dysphagia we have observed when performing fundoplication in these patients.
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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 reflux 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.
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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. Though 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.