Practical Approaches to the Surgical Management of Achalasia

By Finley, Richard J Rattenberry, Jennifer; Clifton, Joanne C; Finley, Christian J; Yee, John

Achalasia is a primary motor disorder of the esophagus characterized by an abnormal hypertensive, nonrelaxing lower esophageal sphincter (LES) and nonfunctioning, aperistaltic esophageal body resulting in significant regurgitation and dysphagia. The primary goal of treatment is palliation of symptoms. At present, all treatment techniques are directed at relieving the functional obstruction at the level of the LES by disruption or paralysis of the esophageal muscle constituting the LES. Destruction of the LES function also places the patient at risk for pathologic gastroesophageal reflux disease. Therefore, the treatment of patients with achalasia must strike a balance between the relief of dysphagia and potential creation of pathologic gastroesophageal reflux. The advent of laparoscopic esophageal myotomy for the treatment of achalasia over the past decade has resulted in most patients with the disease being referred to surgeons for definitive treatment. At the time of consultation the patient may present with a myriad of symptoms, investigative results, and previous treatments. Based on our experience of over 300 patients treated with surgery at our institution between 1990 and 2007, this review will address the practical problems encountered in the surgical management of achalasia. ACHALASIA IS A MOTILITY disorder of the esophagus of uncertain etiology characterized manometricalIy by increased basal lower esophageal sphincter (LES) pressure with incomplete relaxation of the sphincter upon swallowing and aperistalsis of the body of the esophagus. The dysmotility of the LES results in a functional obstruction at the esophagogastric junction, and an esophagus that fails to clear swallowed liquids and solids. Progressive dysphagia to liquids and solids is the primary symptom. Regurgitation and weight loss develop without adequate treatment.

Primary achalasia is most commonly seen in North America and Europe. The underlying pathophysiology seems to be loss of ganglion cells in the myenteric plexus of the esophagus, resulting in absence of peristalsis of the esophageal body, failure of the LES to relax with swallowing, and normal or elevated LES pressures.1 The estimated incidence of primary achalasia is about one case/200,000 population.2 The disorder is most commonly diagnosed in patients between the ages of 20 and 40 years. Achalasia, secondary to ganglion cell destruction by Trypanosoma cruzi infection (Chagas’ disease), is seen primarily in South and Central America. In the endemic areas, Chagas’ megaesophagus develops in one patient/1000 population.3, 4

The primary goal of treatment is palliation of symptoms. At present, all forms of treatment are directed at relieving the functional obstruction at the level of the LES by disruption or poisoning of the muscular fibers. The LES is the primary barrier to gastroesophageal reflux, and so its disruption places the patient at risk for pathologic reflux. The treatment of patients with achalasia must safely ensure the relief of dysphagia, while minimizing the potential creation of pathologic gastroesophageal reflux.

The advent of laparoscopic esophageal myotomy for the treatment of achalasia over the past decade has resulted in most patients with the disease being referred to surgeons for definitive treatment. At the time of consultation, the patient may present with a myriad of symptoms, investigative results, and previous treatments. Based on our experience of over 300 patients treated with surgery at our institution between 1990 and 2007, this review will address the practical problems encountered in the surgical management of achalasia.

Diagnosis

Clinical Features

The functional obstruction at the esophagogastric junction results in symptoms of progressive dysphagia for liquids and solids. The disease usually follows an indolent course, with several years of progressive dysphagia for liquids and solids, leading eventually to regurgitation of undigested food, weight loss, wheezing, and coughing. Over time, the esophagus slowly dilates and eventually assumes a sigmoid appearance on the barium radiograph. Burning retrosternal discomfort, secondary to acidic fermentation products of retained food, may occur at this stage. Patients with vigorous achalasia may have intermittent bouts of crushing retrosternal chest pain. Patients present for medical care with an average duration of symptoms of 6 years.5 In our experience, the frequency of symptoms at the time of surgical consultation are dysphagia (98%), regurgitation (92%), weight loss (71%), heartburn (58%), and aspiration (11%).

Investigation

Early in the disease process, the chest radiograph may be normal. Later, however, manifestations of achalasia may include a widened mediastinum, an airfluid level, absence of a gastric air bubble, and even aspiration pneumonitis. A barium swallow shows absence of peristalsis in the body of the esophagus with distal esophageal narrowing to form a “bird’s beak” configuration. A sigmoid appearance of the esophagus, retention of food, and an esophageal diameter greater than 6 cm are signs of long-standing achalasia.

Upper gastrointestinal endoscopy is used to examine the esophageal mucosa for signs of esophageal cancer and the esophagogastric junction to determine whether there is any structural cause of the obstruction, such as cancer or peptic stricture, which may mimic achalasia. The endoscopist should be able to pass the tube through the esophagogastric junction with minimal pressure in classic achalasia. For biopsy of the esophagogastric junction, the instrument should be directed posteriorly, if possible, to avoid mucosal perforation in the line of the future anterior esophageal myotomy.

Radionucleotide swallows to assess esophageal transit are useful in the diagnosis and follow-up of patients with achalasia. Studies with liquid radionucleotide swallows are more reproducible than solid scintigraphic studies, which have decreased reliability because of poor mixing of the radionucleotide. The esophageal transit time for liquids and solids should be decreased in patients with achalasia in the supine and upright positions.6

Esophageal manometry is the procedure of choice for the diagnosis of achalasia. Classic esophageal manometric findings include: 1) an elevated LES pressure, 2) failure of the LES to relax upon swallowing, and 3) aperistalsis of the body of the esophagus. Absence of peristalsis of the body must be documented to confirm the diagnosis of primary achalasia.7 Patients with vigorous achalasia have high-amplitude, nonperistaltic contractions in the body of the esophagus in response to swallowing and complain more often of chest pain.8, 9

In our center, the patient’s quality of life is assessed by standardized questionnaires, administered in the preoperative period and at 3, 6, and 12 months, and then yearly after surgery.10 Recently, Urbach et al.11 have introduced a patient derived quality of life tool to assess the impact of achalasia and its treatments on quality of life outcomes.

Management

The primary goal of therapy is palliation of symptoms, because the esophageal motor abnormality remains unchanged after all forms of intervention. At present, all treatment techniques are directed at relieving the functional obstruction at the level of the LES by disruption or paralysis of the esophageal muscle constituting the LES. Destruction of the LES function also places the patient at risk for pathologic gastroesophageal reflux disease. Therefore, the treatment of patients with achalasia must strike a balance between the relief of dysphagia and potential creation of pathologic gastroesophageal reflux.

Medical Therapy

Treatment approaches have involved both surgical and nonsurgical techniques. The nonsurgical techniques have consisted of passive esophageal bougienage or pneumatic dilatation of the esophagogastric junction and injection of botulinum toxin into the LES muscles.

Pneumatic dilatation forcibly disrupts the muscular fibers of the LES while preserving the esophageal mucosa. This procedure resulted in esophageal perforation in up to four per cent of patients in one series12 and other significant complications in more than 30 per cent in another series.13 Long-term symptomatic relief of dysphagia and regurgitation is obtainable, with experienced clinicians, in 60 per cent to 75 per cent of patients after the first dilatation and in up to 85 per cent after an additional procedure.8 In a prospective randomized trial however, Csendes et al.14 demonstrated that esophagomyotomy of the muscles constituting the LES via laparotomy controlled dysphagia better compared with pneumatic dilatation.

Endoscopic botulinum toxin injections relaxed the smooth muscle fibers of the pathologic LES, but these effects lasted less than 6 months in most patients. Repeated injections were required for consistent longterm relief.15 Many of these patients require other forms of treatment, and the technique is now limited to poor candidates for either pneumatic dilatation or a surgical procedure.16 Preoperative pneumatic dilatation does not adversely effect the results of an esophageal myotomy. However, patients who have had good relief of symptoms with injection of botulinum into the LES, have a higher intraoperative mucosal perforation rate and less improvement of their dysphagia with esophageal myotomy.17 Treatment with pneumatic dilatation or botulinum injection of the LES should be limited to patients who cannot safely undergo a laparoscopic esophageal myotomy Surgical Therapy

Surgical therapy for achalasia has been directed at obliterating the dysfunctional LES. A myotomy of the muscles of the lower esophagus and gastroesophageal junction using both anterior and posterior incisions was first performed by the German surgeon E. Heller on April 14, 1913.18 The procedure was later modified to a single incision by Groenvedeldt19 and Zaaijer.20

The surgical approach, transabdominal or transthoracic, and the need for an antireflux procedure remain controversial issues. In 1962, Professor Jacques Dor21 at the University of Marseilles described fixing the myotomized lower esophagus in the abdomen and wrapping it using a partial anterior gastric fundoplication to compress the esophagus during elevated intragastric pressure, at which time gastroesophageal reflux usually occurs. Partial fundoplication is preferred to 360-degree fundoplication because a total fundoplication defeats the principle of lowering the high- pressure zone at the bottom of the aperistaltic esophagus. Bonavina et al.22 have reported symptomatic long-term (5-year) improvement in 94 per cent of their patients using an open transabdominal Heller myotomy and anterior fundoplication using the Dor technique.

Long-term symptomatic improvement has been reported after an esophageal myotomy performed through a left thoracotomy, with and without an antireflux procedure. Ellis23 reported that 74 per cent of his patients had no or minimal dysphagia 9 years after a left thoracotomy and myotomy without an antireflux procedure. Malthaner et al.24 reported that 67 per cent of their patients had minimal dysphagia 19 years after a left thoracotomy with partial fundoplication.

After the popularization of minimally invasive surgery, Pellegrini et al.25 reported the first use of thoracoscopic esophagomyotomy for achalasia. A followup of these thoracoscopic esophagomyotomies showed complete relief of dysphagia in 17 of 24 patients and partial relief in four of the 24 patients.26 Five of eight patients tested in the study had experienced abnormally prolonged exposure to acid in the distal esophagus. In our center, two of the first seven patients treated with this technique had an inadequate thoracoscopic myotomy because of inability to carry the myotomy onto the stomach. Stewart et al.27 has shown that laparoscopic myotomy results in less mucosal perforations, postoperative dysphagia, and gastroesophageal reflux than the thoracoscopic approach. Rosati et al.28 first reported excellent relief of symptoms after a laparoscopic myotomy and anterior partial fundoplication for achalasia. The increased incidence of inadequate myotomy and gastroesophageal reflux with thoracoscopic myotomy has led us to favor laparoscopic Heller’s myotomy for the primary surgical therapy of achalasia.

Preoperative Preparation

Patients with achalasia usually present for surgical consideration with signs and symptoms of dysphagia for liquids and solids, regurgitation, weight loss, and aspiration. Severe malnutrition is treated with at least 10 days of enteral feeding before surgical intervention. Cardiopulmonary function is maximized and pulmonary sepsis is cleared before surgery. All patients receive a liquid diet for 2 days before the operation and fast for 12 hours before surgery. At the time of the operation, the esophagus and the stomach are cleaned out with endoscopy before intubation and ventilation to avoid aspiration.

Surgical Procedures

Patients undergoing endoscopic esophageal myotomy should understand the risks and benefits of both laparoscopic and thoracoscopic approaches. Patients who have received a previous botulinum injection are warned about the increased frequency of mucosal perforation related to submucosal fibrosis.17 However, previous botulinum injection should not be a contraindication to endoscopic Heller myotomy.27

The laparoscopic approach is preferred because of the superior long-term results,17,28 but may not be possible if adhesions from previous upper abdominal surgery or infection prevent adequate exposure of the esophagogastric junction. In these cases, the thoracoscopic approach may be necessary. Thoracoscopic myotomy should be limited to patients with extensive abdominal adhesions that preclude a laparoscopic approach or to patients with diffuse esophageal spasm who do not need complete division of the LES or to some patients requiring reoperation for persistent or recurrent dysphagia after laparoscopic esophageal myotomy. In these situations, left thoracotomy may be necessary if adequate exposure of the esophagogastric junction is not possible. Conversely, thoracoscopic surgery may be contraindicated in patients with decreased pulmonary function that prevents the use of one-lung ventilation, which is necessary for accurate visualization of the esophagus.

As a result of experience gained with laparoscopic antireflux procedures and our disappointing results with the thoracoscopic approach, we began to use a laparoscopic approach to perform a Heller myotomy in 1994.6 Since that time, 274 patients with classic achalasia have undergone a primary laparoscopic myotomy of the distal 6 cm of esophagus and the proximal 2 cm of the stomach. Intraoperative esophagogastroscopy facilitates the myotomy and ensures an adequate myotomy. In the preoperative period, 107 patients underwent pneumatic dilatation and 28 had botulinum injection of the LES. None of the patients required conversion to open laparotomy. Two patients had mucosal perforations on the gastric side of the myotomy that were repaired laparoscopically at the time of the initial surgery. In the postoperative period, there were no esophageal leaks and no deaths. One patient required a chest tube for a symptomatic pneumothorax, nine patients had evidence of atelectasis, and one patient had symptomatic delayed gastric emptying. In the early postoperative period, 96 per cent of patients were satisfied with their operation and 80 per cent gained weight. Four patients had persistent daily dysphagia. Twenty patients were taking proton pump inhibitors for symptomatic heartburn. The 145 patients who underwent an anterior fundoplication had a lower incidence of heartburn but a higher rate of postoperative dysphagia than the 129 who did not have a fundoplication. At longest follow- up, 91 per cent of patients were satisfied with the outcome of the procedure.

An adequate myotomy mat obliterates the entire lower esophageal sphincter is most likely to improve esophageal emptying in achalasia patients. Oelschlager et al.29 showed that an extended gastric myotomy (3 cm) more effectively disrupts the lower esophageal sphincter, thus improving the results of surgical therapy for achalasia regarding dysphagia, without increasing the rate of abnormal gastroesophageal reflux, provided that a Toupet fundoplication is added.

Surgical treatment of achalasia with myotomy of the lower esophageal sphincter requires a fine balance between an improvement in esophageal emptying and the possible development of gastroesophageal reflux disease. In a prospective, randomized, double-blind, controlled clinical trial, Richards et al.30 showed that Heller myotomy plus Dor anterior fundoplication was superior to Heller myotomy alone in regard to the incidence of postoperative gastroesophageal reflux as measured by 24 hour pH studies. In a retrospective study of 149 patients, Rice et al.31 showed that gastroesophageal reflux measured by 24 hour pH studies was significantly less in both the upright and supine positions with the addition of a Dor fundoplication to laparoscopic Heller myotomy. Lower premyotomy LES pressure was associated with increased reflux in both of these studies. The abnormal 24 hour pH studies seen in the patient groups without fundoplication are just above the upper limits of normal. Although the long term effects of this low exposure to acid is unknown, these patients should probably be treated with proton pump inhibitors to reduce the long term sequelae of peptic strictures or columnar lined esophagus.

Conversely, the addition of a fundoplication to prevent reflux may adversely affect esophageal emptying after esophageal myotomy. The addition of a Nissen fundoplication to Heller myotomy failed to improve esophageal emptying immediately postmyotomy. Furthermore, esophageal emptying worsened over time, with 29 per cent of patients requiring takedown of the Nissen fundoplication.32 Finley et al.33 showed that patients with an anterior fundoplication after myotomy had decreased esophageal clearance and less improvement in dysphagia and regurgitation scores compared with patients without fundoplication. Other studies showed that the addition of fundoplication increased resting and residual LES pressures compared with no fundoplication but did not significantly effect esophageal emptying, as assessed by timed barium31 or increase the incidence of dysphagia. Pending long term follow-up, the present evidence suggests that the optimal laparoscopic operation involves complete obliteration of the LES with an extended gastric myotomy followed by a loose anterior or posterior partial fundoplication.

Postoperative Care

An esophagogram with water-soluble contrast material is obtained on the first postoperative day to rule out mucosal perforations. A clear fluid diet is started, and the patient is discharged to home, usually within 24 to 48 hours. Patients are given a dental soft diet for 3 weeks postoperatively, after which a normal diet is resumed.

Management of Persistent or Recurrent Symptoms

Patients with persistent or recurrent dysphagia may be treated with balloon dilatation up to 20 mm in diameter without significant risk of esophageal perforation. If symptoms persist the patient should be reinvestigated with a barium swallow, esophagogastroscopy, and esophageal manometry. Patients may require reoperation for significant dysphagia due to an inadequate myotomy or stricturing. In our center, four of our 274 patients and five patients who received their operations at another institution have undergone reoperation. Two of our patients underwent laparoscopic takedown of the anterior fundoplication for persistent dysphagia. Two of our patients and two outside patients underwent thoracoscopic esophageal myotomy for recurrent stricturing with good results. Three patients who had a transthoracic esophageal myotomy in the past had a laparoscopic esophageal myotomy carried on to the stomach with good relief of dysphagia. Patti et al.34 studied 133 patients who had undergone a laparoscopic myotomy in addition to a partial fundoplication. Mucosal perforations, which occurred in six patients, were closed laparoscopically. Eleven per cent of the patients had persistent dysphagia initially, and one per cent developed recurrent dysphagia after 1 year. Four of these patients had imperfectly formed Dor fundoplications, five had fibrotic transmural strictures, and two had incomplete myotomies. The incidence of preventable technical failure dropped from 23 per cent during the early period of the study to 3 per cent in the later experience. New gastroesophageal reflux developed in 17 per cent of patients after laparoscopic myotomy. However, preoperative reflux was corrected in five of seven patients. The authors also reported excellent swallowing after a laparoscopic Heller myotomy, even in patients with an esophageal diameter greater than 6 cm. The ability to mobilize and straighten a sigmoid-shaped esophagus during laparoscopic myotomy may improve esophageal emptying.

Since 1994, none of our patients undergoing a primary laparoscopic esophageal myotomy have required an esophagectomy. Patients who have weight loss or aspiration secondary to end-stage megaesophagus, failure of prior myotomy, or associated reflux stricture may benefit from an esophagectomy. Devaney et al.35 has shown that transhiatal esophagectomy and gastric interposition may be carried out with reasonable morbidity and mortality and good long term quality of life.

Conclusion

To ensure optimal results, a definitive diagnosis of classic achalasia needs to be established before dierapy. For primary surgical therapy of achalasia, complete obliteration of the LES with a laparoscopic myotomy of the distal 6 cm of esophagus and the proximal 2 to 3 cm of the stomach is a safe and effective method to reduce the symptoms of dysphagia aand regurgitation. A loose anterior or posterior partial fundoplication decreases acid exposure to the esophagus and may reduce the long term sequelae of peptic stricture and columnar lined esophagus. Preoperative treatment with pneumatic dilatation or botulinum injection of the LES are not a contraindication to laparoscopic esophageal myotomy, but their use should be limited to patients who cannot safely undergo a laparoscopic esophageal myotomy. Reoperation for persistent symptoms should depend on the underlying pathology and previous approaches to surgery.

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RICHARD J. FINLEY, M.D., JENNIFER RATTENBERRY, B.SC, M.SC, JOANNE C. CLIFTON, B.A., M.SC,

CHRISTIAN J. FINLEY, M.D., JOHN YEE, M.D.

From the Division of Thoracic Surgery, Department of Surgery, University of British Columbia,

and the Vancouver Hospital, Vancouver, British Columbia

Address correspondence and reprint requests to Richard J. Finley, M.D., Department of Surgery, The University of British Columbia, Faculty of Medicine, 910 West 10th Avenue, 3rd Floor, Vancouver, B.C. V5Z 4E3. E-mail: rjfinley@shaw.ca.

Copyright Southeastern Surgical Congress Feb 2008

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