INTRODUCTION

Achalasia is a rare, acquired disorder characterized by the triad of aperistalsis of the esophagus, a hypertonic lower esophageal sphincter (LES), and a failure of LES relaxation in response to swallowing.¹ The primary pathophysiology in LES hypertension is related to the destruction of myenteric ganglion cells via an inflammatory, possibly infectious, mechanism.² This process leads to hypertonicity of the LES and its failure to relax normally in response to swallowing. The resulting functional obstruction, which causes dysphagia, leads with time to abnormal dilation of the more proximal esophagus. In fact, the abnormalities seen in the peristalsis of the esophagus may be solely a secondary phenomenon related to its prolonged abnormal distention.²

The “gold standard” for diagnosing achalasia, after an appropriate history and physical examination has suggested the disease process, is esophageal manometry, revealing the triad described previously. Some physicians choose to start with a barium swallow,² which can suggest achalasia as well as evaluate for other disease processes and anatomic variations that may make endoscopy/manometry more difficult. An esophagogastroduodenoscopy (EGD), however, is essential in the preoperative work-up to evaluate not only for other disease processes such as malignancy or a stricture (both potential causes of pseudoachalasia) but also anatomy. Any suspicion of pseudoachalasia related to a malignant process warrants a computed tomography (CT) scan and other work-up as appropriate.

Although multiple nonsurgical treatment modalities for achalasia exist, none is as effective as definitive surgical esophagomyotomy, usually performed via a minimally invasive technique. The response to pharmacologic agents such as calcium channel blockers and nitrates is usually poor and short-lived.² Furthermore, nonsurgical interventions, such as forceful endoscopic dilation of the LES and LES botulinum toxin injection, are not without risk. Okike and coworkers³ found that the risk of esophageal leak and mediastinal sepsis was four times higher in those patients undergoing endoscopic forceful dilation than in those treated with surgical esophagomyotomy. In addition, these interventions often increase the difficulty and morbidity of subsequent surgical myotomy^1,4,5 and can also decrease the effectiveness of the procedure.²

The significant reduction in operative morbidity afforded by minimally invasive surgery has increased the attractiveness of surgical esophagomyotomy over nonsurgical procedures. Both video-assisted thoracic surgery (VATS) and laparoscopic approaches are options, but studies have suggested that the latter is associated with a shorter hospital stay, decreased conversion rate, and better relief of dysphagia.^6,7 Most series report a success rate of approximately 90% or higher in relieving symptoms with laparoscopic esophagomyotomy.^1,4,8 This compares quite favorably with the long-term success seen with botulinum toxin injection or pneumatic dilation. Most patients who receive botulinum toxin injections do not achieve long-term relief, and the long-term success rate of pneumatic dilation is only about 65% to 70%.^2,9

Although the majority of patients who undergo laparoscopic esophagogastric myotomy obtain excellent symptom relief, the procedure is not without complications. The operative mortality is low (e.g., <0.5%), if not zero, in most series. The most common serious complication, especially if not identified and repaired, is esophageal or gastric injury with immediate or delayed perforation. Other complications to be discussed include persistent or recurrent dysphagia, gastroesophageal reflux disease (GERD), bleeding, and paraesophageal hernia.

INDICATIONS

OPERATIVE STEPS

OPERATIVE PROCEDURE

Endoscope Placement

Many surgeons place an endoscope at the GEJ prior to beginning the procedure. This not only allows for endoscopic identification of the GEJ (squamocolumnar junction) but also is helpful in assessing the mucosa and myotomy after the dissection. The lighted endoscope, with the aid of insufflation, allows for inspecting the mucosa for small injuries or for residual uncut muscle fibers overlying the mucosa (Figs. 18-1 and 18-2). Endoscopy is also useful in assessing the adequacy of the myotomy. To that end, some have even advocated intraoperative manometry to ensure the absence of residual high-pressure zones of the GEJ.⁹

Figure 18-1 Note the presence of residual muscle fibers overlying the mucosa (black arrow), preventing complete separation of the myotomy edges (white arrows) in this segment.

Figure 18-2 Residual muscle fibers constrict the otherwise bulging mucosa. Failure to divide these fibers (often visually less obvious than illustrated here) will lead to persistent postoperative dysphagia.

Takedown of the Anterior Phrenoesophageal Ligament and Anterior Dissection into the Mediastinum

Paraesophageal Hernia

In contrast to the dissection performed in an antireflux procedure or takedown of a hiatal/paraesophageal hernia, the hiatal dissection should ideally remain limited in laparoscopic Heller myotomy.^9,10

• Consequence

In gaining exposure to the anterior aspect of the GEJ, not only is extensive (i.e., circumferential) dissection usually unnecessary, but it also alters the GEJ physiologically and thereby may predispose to reflux. Furthermore, Chapman and associates⁹ described a postoperative paraesophageal hernia as a complication they encountered with laparoscopic myotomy, which necessitated repeat operation for repair.

Grade 2/3 complication

• Repair

One should inspect the hiatus after completion of the procedure to ensure that it is not excessively loose. The presence of a hiatal hernia or a shortened “sigmoid” esophagus, for example, may necessitate more thorough dissection around the GEJ than would normally be required. If the hiatal opening appears loose, it should be corrected with posterior crural sutures, keeping in mind that dysphagia may result from a too-tight closure.

• Prevention

Whereas some dissection is needed to expose the esophagus for an effective myotomy, this should mainly be performed anteriorly,¹¹ with a minimum of lateral and posterior dissection. However, some make a small opening posterior to the esophagus in order to place a Penrose drain for traction.⁹ Regardless, the size of the hiatus and the potential for herniation must be assessed prior to closure (Fig. 18-3). This is particularly true if a significant amount of dissection has been necessary, for example, in those patients with advanced disease and resulting “sigmoid” or shortened esophagus.¹²

Figure 18-3 The rather large hiatal opening in this patient predisposes to postoperative gastroesophageal reflux (GER) and paraesophageal hernia. Sutures are placed in the posterior aspects of the crura to minimize these risks (the first suture is shown).

Vagal Nerve Injury

See later and Section III, Chapter 17, Laparoscopic Nissen Fundoplication.

Esophageal Injury

See later and Section III, Chapter 17, Laparoscopic Nissen Fundoplication.

Pneumothorax, Pneumomediastinum, and Pneumopericardium

See Section III, Chapter 17, Laparoscopic Nissen Fundoplication.

Ligation of the Short Gastric Vessels

Ligation of the short gastric vessels allows for gastric mobilization such that the fundoplication can be performed.¹ We perform complete ligation of the short gastric vessels with the harmonic scalpel. Others advocate limiting this dissection to the more cephalad short gastric vessels,^1,9 presumably in the interest of minimizing disruption of the LES/GEJ physiology. Regardless, usually at least some of the short gastric vessels must be ligated in order to provide enough mobility of the proximal fundus to complete a fundoplication.

Bleeding

See Section III, Chapter 17, Laparoscopic Nissen Fundoplication.

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