Formation of the Gut Tube

During the embryonic period of development, cephalocaudal (Fig. 43-1) and lateral folding of the embryo occurs. As a result, a portion of the endoderm-lined yolk sac cavity is incorporated into the embryo to form the primitive gut. The primitive gut forms a blind-ending tube consisting of the foregut, midgut, and hindgut (Fig. 43-2). The foregut gives rise to the esophagus. It extends from the pharyngeal tube as far caudally as the liver outgrowth. By the end of week 3 of development, the primitive foregut develops a ventral diverticulum from which the tracheobronchial tree develops. The tracheoesophageal septum gradually partitions this diverticulum from the dorsal portion of the foregut, resulting in a ventral respiratory primordium and dorsal esophagus (Fig. 43-3). During weeks 4 and 5 of development, the rapid growth of the heart and liver allows the esophagus to stretch. As it elongates, the esophageal lumen is almost completely obliterated at the level of the carina. The dorsal esophageal embrace of the trachea results in close approximation of the tracheal bifurcation to the front wall of the esophagus, further narrowing the esophageal lumen.

FIGURE 43-1 Early embryologic development.

(Adapted from Pearson FG, Cooper JD, Deslauriers J, et al: Esophageal surgery, ed 2, New York, 2002, Churchill Livingstone, p 20.)

FIGURE 43-2 The developing gut.

FIGURE 43-3 Partitioning of the foregut. A, Week 4; B, week 8; C, week 14

(Adapted from Sadler TW [ed]: Medical embryology, Philadelphia, 2003, Lippincott Williams & Wilkins, p 290.)

Molecular Regulation of the Gut Tube

Differentiation of various regions of the gut and its derivatives is dependent on a reciprocal interaction between the endoderm (epithelium) of the gut tube and surrounding splanchnic mesoderm. The mesoderm dictates the type of structure that will form, such as the esophagus forming from the foregut, through an HOX code. The induction of the HOX code is a result of sonic hedgehog (SHH) that is expressed throughout the gut endoderm. In the foregut, expression of SHH in the endoderm promotes the expression of the HOX code in the mesoderm. Once specified by this code, the mesoderm instructs the endoderm to form the various components of the foregut.²

Differentiation of the Endoderm

Early in gestation the mesoderm is HOX-coded to instruct the endoderm to form the epithelial lining of the digestive tract. At the end of the embryonic period, from weeks 6 to 8 of gestation, the epithelium becomes two to five cells thick and remains stratified columnar epithelium. During the week 10 of development, stratified columnar epithelium becomes ciliated. By week 12, the epithelium is completely ciliated and growth is taking place only at the basal level. During months 4 and 5 of gestation, stratified squamous epithelium replaces the ciliated columnar epithelium.

Muscular Development from the Mesoderm

The remainder of the esophagus is formed from the mesoderm. By week 6 of gestational development, the esophagus is surrounded by a layer of undifferentiated mesoderm and a circular layer of myoblasts. Longitudinal muscle fibers appear in the lower esophagus as the circular layer of muscle becomes well established. The smooth muscle that forms the lower two thirds of the esophagus arises from the splanchnic mesoderm and is innervated by the splanchnic plexus. The striated muscle of the upper esophagus is derived from the caudal branchial arches and appears from weeks 12 to 15. It will eventually be innervated by the vagus nerve. Muscular proliferation peaks during weeks 11 and 12, so that by week 12 of gestation, the longitudinal muscle is well defined. Ganglion cells also appear in the myenteric plexus, whereas the longitudinal muscle becomes well defined between weeks 10 and 12 of gestation. Furthermore, the muscularis mucosa becomes well defined, and typical mucosal folds formed by longitudinal mesenchymal ridges can be appreciated.

Growth of the esophagus continues at a slower pace after morphologic changes have concluded. On a functional level, swallowing first appears at week 14 and is well established by the end of month 4 of gestation.

Esophageal Inlet

The high-pressure zone at the inlet of the esophagus is the UES, which anatomically marks the end of a complex configuration of muscles that begins in the larynx and posterior pharynx and ends in the neck. The pharyngeal constrictor muscles are three consecutive muscles that begin at the base of the palate and end at the crest of the esophagus. The superior and middle pharyngeal constrictor muscles, as well as the oblique, transverse, and posterior cricoarytenoid muscles, are immediately proximal to the UES and serve to anchor the pharynx and larynx to structures in the mouth and palate. These muscles also aid in deglutition and speech, but are not responsible for the high pressures noted in the UES. The inferior pharyngeal constrictor muscle is the final bridge between the pharyngeal and esophageal musculature.

Inserting into the median pharyngeal raphe, the inferior pharyngeal constrictor muscle is composed of two consecutive muscle beds—the thyropharyngeus and cricopharyngeus muscles—that originate bilaterally from the lateral portions of the thyroid and cricoid cartilages, respectively. The transition between the oblique fibers of the thyropharyngeus muscle and the horizontal fibers of the cricopharyngeus muscle creates a point of potential weakness, known as Killian’s triangle (site of a Zenker’s diverticulum). The cricopharyngeus muscle is responsible for generating a high-pressure zone that marks the position of the UES and esophageal introitus. Its distinctive bowing array of muscle fibers is unique and serves to transition into the circular esophageal musculature. This point of transition is flanked by the longitudinal esophageal muscles that extend superiorly to attach to the midportion of the posterior surface of the cricoid cartilage and form the V-shaped area of Laimer.

Esophageal Layers

The esophagus is comprised of two proper layers, the mucosa and muscularis propria. It is distinguished from the other layers of the alimentary tract by its lack of a serosa. The mucosa is the innermost layer and consists of squamous epithelium for most of its course. The distal 1 to 2 cm of esophageal mucosa transitions to cardiac mucosa or junctional columnar epithelium at a point known as the Z-line (Fig. 43-5). Within the mucosa, there are four distinct layers—the epithelium, basement membrane, lamina propria, and muscularis mucosae. Deep to the muscularis mucosae lays the submucosa (Fig. 43-6). Within it is a plush network of lymphatic and vascular structures, as well as mucous glands and Meissner’s neural plexus.

FIGURE 43-5 Z-line.

FIGURE 43-6 Layers of the esophagus.

(Adapted from Pearson FG, Cooper JD, Deslauriers J, et al: Esophageal surgery, ed 2, New York, 2002, Churchill Livingstone, p 124.)

Enveloping the mucosa, directly abutting the submucosa, is the muscularis propria. Below the cricopharyngeus muscle, the esophagus is composed of two concentric muscle bundles, an inner circular and outer longitudinal (Fig. 43-7). Both layers of the upper third of the esophagus are striated, whereas the layers of the lower two thirds are smooth muscle. The circular muscles are an extension of the cricopharyngeus muscle and traverse through the thoracic cavity into the abdomen, where they become the middle circular muscles of the lesser curvature of the stomach. The collar of Helvetius marks the transition of the circular muscles of the esophagus to oblique muscles of the stomach at the incisura (cardiac notch). Between the layers of esophageal muscle is a thin septum comprised of connective tissue, blood vessels, and an interconnected network of ganglia known as Auerbach’s plexus. Enshrouding the inner circular layer, the longitudinal muscles of the esophagus begin at the cricoid cartilage and extend into the abdomen, where they join the longitudinal musculature of the cardia of the stomach. The esophagus is then wrapped by a layer of fibroalveolar adventitia.

FIGURE 43-7 Muscles of the esophagus.

Anatomic Narrowing

The esophageal silhouette resembles an hourglass. There are three distinct areas of narrowing that contribute to its shape. Measuring 14 mm in diameter, the cricopharyngeus muscle is the narrowest point of the gastrointestinal tract and marks the superiormost portion of the hourglass-shaped esophagus. Located just below the carina, where the left mainstem bronchus and aorta abut the esophagus, the bronchoaortic constriction at the level of the fourth thoracic vertebra creates the center narrowing and measures 15 to 17 mm. Finally, the diaphragmatic constriction, measuring 16 to 19 mm, marks the inferior portion of the hourglass and is located where the esophagus passes through the diaphragm. Between these three distinct areas of anatomic constriction are two areas of dilation known as the superior and inferior dilations. Within these areas, the esophagus resumes the normal diameter for an adult and measures approximately 2.5 cm.

Gastroesophageal Junction

The UES and LES mark the entrance and exit to the esophagus, respectively. These sphincters are defined by a high-pressure zone but can be difficult to identify anatomically. The UES corresponds reliably to the cricopharyngeus muscle, but the LES is more complex to discern. There are four anatomic points that identify the gastroesophageal junction (GEJ), two endoscopic and two external. Endoscopically, there are two anatomic considerations that may be used to identify the GEJ. The squamocolumnar epithelial junction (Z-line) may mark the GEJ provided that the patient does not have a distal esophagus replaced by columnar-lined epithelium, as seen with Barrett’s esophagus. The transition from the smooth esophageal lining to the rugal folds of the stomach may also identify the GEJ accurately. Externally, the collar of Helvetius (or loop of Willis), where the circular muscular fibers of the esophagus join the oblique fibers of the stomach, and the gastroesophageal fat pad are consistent identifiers of the GEJ (Fig. 43-8).

FIGURE 43-8 Identifiers of the gastroesophageal junction.

Vasculature

The rich vascular and lymphatic structures that nourish and drain the esophagus serve as a surgical safety net and a highway for metastases. The vasculature is divided into three segments, cervical, thoracic, and abdominal. The cervical esophagus receives most of its blood supply from the inferior thyroid arteries, which branch off of the thyrocervical trunk on the left and the subclavian artery on the right (Fig. 43-9). The cricopharyngeus muscle, which marks the inlet of the esophagus, is supplied by the superior thyroid artery. The thoracic esophagus receives its blood supply directly from four to six esophageal arteries coming off the aorta, as well as esophageal branches off the right and left bronchial arteries. It is supplemented by descending branches off the inferior thyroid arteries, intercostal arteries, and ascending branches of the paired inferior phrenic arteries. The abdominal esophagus receives its blood supply from the left gastric artery and paired inferior phrenic arteries. All the arteries that supply blood to the esophagus terminate in a fine capillary network before they penetrate the muscular wall of the esophagus. After penetrating and supplying the muscular layers, the capillary network continues the length of the esophagus within the submucosal layer.

FIGURE 43-9 Arterial supply to the esophagus.

The venous drainage parallels the arterial vasculature and is just as complex. In all parts of the esophagus, the rich submucosal venous plexus is the first basin for venous drainage of the esophagus. In the cervical esophagus, the submucosal venous plexus drains into the inferior thyroid veins, which are tributaries of the left subclavian vein and right brachiocephalic vein (Fig. 43-10). The drainage of the thoracic esophagus is more intricate. The submucosal venous plexus of the thoracic esophagus joins with the more superficial esophageal venous plexus and the venae comitantes that envelop the esophagus at this level. This plexus, in turn, drains into the azygos and hemiazygos veins on the right and left sides of the chest, respectively. The intercostal veins also drain into the azygos venous system. The abdominal esophagus drains into the systemic and portal venous systems through the left and right phrenic veins and left gastric (coronary) vein and short gastric veins, respectively.

FIGURE 43-10 Venous drainage of the esophagus.

Lymphatics

The lymphatic drainage of the esophagus is extensive; it consists of two interconnecting lymphatic plexuses arising from the submucosa and muscularis layers. The submucosal lymphatics penetrate the muscularis propria and drain into the plexus that runs longitudinally in the esophageal wall. They then egress and drain into regional lymph node beds. In the upper two thirds of the esophagus, lymphatic flow is upward, whereas in the distal third, flow tends to be downward. Esophageal lymphatics begin in the neck with drainage to the paratracheal lymph nodes anteriorly and deep lateral cervical and internal jugular nodes laterally and posteriorly. Once inside the chest, the lymphatics form a matrix of interconnecting channels that drain into the mediastinal lymph nodes and thoracic duct. Anteriorly, the paratracheal and subcarinal lymph nodes, and the paraesophageal, retrocardiac, and infracardiac nodes, all drain the esophagus.

Other mediastinal stations, such as the para-aortic and inferior pulmonary ligament nodes, can also receive drainage from the thoracic esophagus. Posteriorly, nodes along the esophagus and azygos veins are the primary sites of drainage (Fig. 43-11). The intricate lymphatic network of the esophagus allows for rapid spread of infection and tumor into three body cavities. It stands to reason that the rich arterial supply to the esophagus makes it one of the more durable organs in the body with respect to surgical manipulation, whereas its comprehensive venous and lymphatic drainage create an oncologic challenge to controlling cellular migration. These anatomic complexities lead to surgical challenges when treating esophageal cancer and other esophageal diseases.

FIGURE 43-11 Lymphatic drainage of the esophagus.

Innervation

The innervation to the esophagus is sympathetic and parasympathetic (Fig. 43-12). The cervical sympathetic trunk arises from the superior ganglion in the neck. It extends next to the esophagus into the thoracic cavity, where it terminates in the cervicothoracic (stellate) ganglion. Along the way, it gives off branches to the cervical esophagus. The thoracic sympathetic trunk continues on from the stellate ganglion, giving off branches to the esophageal plexus, which envelops the thoracic esophagus anteriorly and posteriorly. Inferiorly, the greater and lesser splanchnic nerves innervate the distal thoracic esophagus. In the abdomen, the sympathetic fibers lay posteriorly alongside the left gastric artery.

FIGURE 43-12 Innervation of the esophagus.

The parasympathetic fibers arise from the vagus nerve, which gives rise to the superior and recurrent laryngeal nerves. The superior laryngeal nerve branches into the external and internal laryngeal nerves that supply motor innervation to the inferior pharyngeal constrictor muscle and cricothyroid muscle and sensory innervation to the larynx, respectively (Fig. 43-13). The right and left recurrent laryngeal nerves come off the vagus nerve and loop underneath the right subclavian artery and aortic arch, respectively. They then travel upward in the tracheoesophageal groove to enter the larynx laterally underneath the inferior pharyngeal constrictor muscle. Along the way, they innervate the cervical esophagus, including the cricopharyngeus muscle. Unilateral injury to the superior or recurrent laryngeal nerve results in hoarseness and aspiration from laryngeal and UES dysfunction. In the thorax, the vagus nerve sends fibers to the striated muscle and parasympathetic preganglionic fibers to the smooth muscle of the esophagus. A weblike nervous plexus envelops the esophagus throughout its thoracic extent. These sympathetic and parasympathetic fibers penetrate through the muscular wall, forming networks between the muscle layers to become Auerbach’s plexus and within the submucosal layer to become Meissner’s plexus (Fig. 43-14). They provide an intrinsic autonomic nervous system within the esophageal wall that is responsible for peristalsis. The parasympathetic fibers coalesce 2 cm above the diaphragm into the left (anterior) and right (posterior) vagus nerves, which descend anteriorly onto the fundus and lesser curvature and posteriorly onto the celiac plexus, respectively.

FIGURE 43-13 Innervation of the larynx.

FIGURE 43-14 Intrinsic esophageal innervation.

Swallowing

There are three phases to swallowing, oral, pharyngeal, and esophageal. Six events occur during the oropharyngeal phase of swallowing (Fig. 43-15). These rapid series of events last about 1.5 seconds and, once initiated, are completely reflexive.

FIGURE 43-15 Phases of oropharyngeal swallowing.

(Adapted from Zuidema GD, Orringer MB: Shackelford’s surgery of the alimentary tract, ed 3, Philadelphia, 1991, WB Saunders, p 95.)

Esophageal Phase

Upper Esophageal Sphincter

The esophageal phase of swallowing is initiated by the actions during the pharyngeal phase. To allow passage of the food bolus, the UES relaxes and the peristaltic contractions of the posterior pharyngeal constrictors propel the bolus into the esophagus. The pressure differential generated between the positive pressure in the cervical esophagus and the negative intrathoracic pressure sucks the bolus into the thoracic esophagus. Within 0.5 second of the initiation of swallowing, the UES closes, reaching close to 90 mm Hg. This postrelaxation contraction lasts 2 to 5 milliseconds, initiates peristalsis, and prevents reflux of the bolus back into the pharynx. The UES pressure returns to resting pressure (60 mm Hg) as the wave travels into the midesophagus (Fig. 43-16).

FIGURE 43-16 Manometry of the upper esophageal sphincter.

(Adapted from Pearson FG, Cooper JD, Deslauriers J, et al: Esophageal surgery, ed 2, New York, 2002, Churchill Livingstone, p 480.)

Peristalsis

There are three types of esophageal contractions, primary, secondary, and tertiary. Primary peristaltic contractions are progressive and move down the esophagus at a rate of 2 to 4 cm/sec and reach the LES about 9 seconds after the initiation of swallowing (Fig. 43-17). They generate an intraluminal pressure from 40 to 80 mm Hg. Successive swallows will follow with a similar peristaltic wave unless swallowing is repeated rapidly, at which time the esophagus will remain relaxed until the last swallow occurs, and peristalsis will follow. Secondary peristaltic contractions are also progressive but are generated from distention or irritation of the esophagus, rather than voluntary swallowing. They can occur as an independent local reflex to clear the esophagus of material that was left behind after the progression of the primary peristaltic wave. Tertiary contractions are nonprogressive, nonperistaltic, monophasic or multiphasic, simultaneous waves that can occur after voluntary swallowing or spontaneously between swallows throughout the esophagus. They represent uncoordinated contractions of the smooth muscle that are responsible for esophageal spasm.

FIGURE 43-17 Normal esophageal peristalsis.

(From Bremner CG, DeMeester TR, Bremner RM, Mason RJ: Esophageal motility testing made easy, St Louis, 2001, Quality Medical Publishing, p 35.)

Lower Esophageal Sphincter

The final phase of esophageal bolus transit occurs through the LES. Although this is not a true sphincter, there is a distinct high-pressure zone that measures 2 to 5 cm in length and generates a resting pressure of 6 to 26 mm Hg. The LES is located in the chest and abdomen. A minimum total length of 2 cm, with at least 1 cm of intra-abdominal length, is required for normal LES function. The transition from the intrathoracic to the intra-abdominal sphincter is noted on a manometric tracing and is known as the respiratory inversion point (RIP; Fig. 43-18). At this point, the pressure of the esophagus changes from negative to positive with inspiration and positive to negative with expiration.

FIGURE 43-18 Normal lower esophageal sphincter.

(From Bremner CG, DeMeester TR, Bremner RM, Mason RJ: Esophageal motility testing made easy, St Louis, 2001, Quality Medical Publishing, p 15.)

Peristaltic contractions alone do not generate enough force to open up the LES. Vagal-mediated relaxation of the LES occurs 1.5 to 2.5 seconds after pharyngeal swallowing and lasts 4 to 6 seconds. This flawlessly timed relaxation is needed to allow efficient transport of a food bolus out of the esophagus and into the stomach. A postrelaxation contraction of the LES occurs after the peristaltic wave has passed through the esophagus, allowing the LES to return to its baseline pressure (Fig. 43-19), reestablishing a barrier to reflux.

FIGURE 43-19 Relaxation of the lower esophageal sphincter.

(From Bremner CG, DeMeester TR, Bremner RM, Mason RJ: Esophageal motility testing made easy, St Louis, 2001, Quality Medical Publishing, p 24.)

Reflux Mechanism

Not all reflux is abnormal. Healthy individuals have occasional episodes of gastroesophageal reflux that is a result of spontaneous opening of the LES. The competence of the LES and its ability to establish a barrier to reflux depends on several factors—adequate pressure and length, radial symmetry, and motility of the esophagus and stomach. A competent sphincter is at least 2 cm and carries a pressure between 6 and 26 mm Hg. Radial asymmetry and abnormal peristalsis prevent proper closure and allow free refluxing of gastric material into the distal esophagus. Abnormal esophageal motility and poor gastric emptying result in inadequate esophageal clearance that also encourages reflux. Finally, neurotransmitters, hormones, and peptides that regulate the LES can increase or decrease tone. All these anatomic and physiologic disruptions can result in reflux through the LES and are implicated in the development of gastroesophageal reflux disease (GERD).

Diverticula

Historically, esophageal diverticula were thought to be a primary disorder that resulted in motility abnormalities. It is now well established that most diverticula are a result of a primary motor disturbance or an abnormality of the UES or LES. Diverticula were originally classified according to their location and, as a convention, they are classifications to which we still adhere. Esophageal diverticula can occur in several places along the esophagus. The three most common sites of occurrence are pharyngoesophageal (Zenker’s), parabronchial (midesophageal), and epiphrenic (supradiaphragmatic). True diverticula involve all layers of the esophageal wall, including mucosa, submucosa, and muscularis. A false diverticulum consists of mucosa and submucosa only. Pulsion diverticula are false diverticula that occur because of elevated intraluminal pressures generated from abnormal motility disorders. These forces cause the mucosa and submucosa to herniate through the esophageal musculature. Both a Zenker’s diverticulum and an epiphrenic diverticulum fall under the category of false pulsion diverticula. Traction, or true, diverticula result from external inflammatory mediastinal lymph nodes adhering to the esophagus as they heal and contract, pulling the esophagus during the process. Over time, the esophageal wall herniates, forming an outpouching, and a diverticulum ensues.

Pharyngoesophageal (Zenker’s) Diverticulum

Originally described by Zenker and Von Ziemssen, the pharyngoesophageal diverticulum (Zenker’s diverticulum) is the most common esophageal diverticulum found today. It usually presents in older patients in the seventh decade of life and has been postulated to be a result of loss of tissue elasticity and muscle tone with age. It is specifically found herniating into Killian’s triangle, between the oblique fibers of the thyropharyngeus muscle and the horizontal fibers of the cricopharyngeus muscle (Fig. 43-20). As the diverticulum enlarges, the mucosal and submucosal layers dissect down the left side of the esophagus into the superior mediastinum, posteriorly along the prevertebral space. Zenker’s diverticulum is often referred to as cricopharyngeal achalasia and is managed accordingly.

FIGURE 43-20 Zenker’s diverticulum.

Symptoms and Diagnosis

Until the Zenker’s diverticulum begins to enlarge, patients are often initially asymptomatic. Commonly, patients complain of a sticking in the throat. A nagging cough, excessive salivation, and intermittent dysphagia often are signs of progressive disease. As the sac increases in size, regurgitation of foul-smelling, undigested material is common. Halitosis, voice changes, retrosternal pain, and respiratory infections are especially common in older adults. Patients learn to compensate for the difficulties by avoiding social situations. The most serious complication from an untreated Zenker’s diverticulum is aspiration pneumonia or lung abscess. In an older patient, this can be morbid and sometimes fatal.

Diagnosis is made by barium esophagraphy (Fig. 43-21). At the level of the cricothyroid cartilage, the diverticulum can be seen filled with barium resting posteriorly alongside the esophagus. Lateral views are critical to obtain because this is usually a posterior structure. Neither esophageal manometry nor endoscopy is needed to diagnose Zenker’s diverticulum.

FIGURE 43-21 Barium swallow showing Zenker’s diverticulum.

(Adapted from Trastek VF, Deschamps C: Esophageal diverticula. In Shields TW, Locicero J III, Ponn RB [eds]: General thoracic surgery, ed 5, Philadelphia, 1999, Lippincott Williams & Wilkins, p 1841.)

Treatment

Surgical or endoscopic repair of a Zenker’s diverticulum is the gold standard of treatment. Traditionally, an open repair through the left neck was advocated. However, endoscopic exclusion has gained popularity in many centers throughout the United States. Two types of open repair are performed, resection and surgical fixation of the diverticulum. The diverticulectomy and diverticulopexy are performed through an incision in the left neck. Under general anesthesia, they both require about 1 hour to complete. In all cases, a myotomy of the proximal and distal thyropharyngeus and cricopharyngeus muscles is performed. In cases of a small diverticulum (<2 cm), a myotomy alone is often sufficient. In frail patients who may be subject to a higher rate of cervical esophageal leak, a diverticulopexy, without resection, may be performed and will prevent symptoms from recurring.³ In most patients with good tissue or a large sac (>5 cm), excision of the sac is indicated. The postoperative stay is approximately 2 to 3 days, during which the patient remains unable to eat or drink.

An alternative to open surgical repair is the endoscopic Dohlman procedure, which has become more popular. Endoscopic division of the common wall between the esophagus and diverticulum using a laser or stapler has also been successful. Because of the configuration of the inline stapling device, this approach has been advocated for larger diverticula. The risk for an incomplete myotomy increases with smaller diverticula, smaller than 3 cm. This method divides the distal cricopharyngeus muscle while obliterating the sac. The esophagus and diverticulum form a common channel. The technique requires maximal extension of the neck and can be difficult to perform in older patients with cervical stenosis. It is done transorally under general anesthesia in approximately 1 hour. The postoperative course is slightly shorter, with patients taking liquids the following day and requiring only a single overnight hospital stay. Thus, this technique has gained favor and is advocated for patients with diverticula between 2 and 5 cm.

The results of open repair versus endoscopic repair have been well studied. For diverticula 3 cm or less in size, surgical repair is superior to endoscopic repair in eliminating symptoms. For any diverticulum larger than 3 cm, the results are the same.⁴ Both the hospital stay and length of inanition are shorter with an endoscopic procedure. Regardless of the method of repair, patients do well and the results are excellent.

Midesophageal Diverticula

Midesophageal diverticula were first described in the 19th century. Historically, inflamed mediastinal lymph nodes from an infection with tuberculosis accounted for most cases (Fig. 43-22). Infections with histoplasmosis and resultant fibrosing mediastinitis have now become more common. Inflammation of the lymph nodes exerts traction on the wall of the esophagus and leads to the formation of a true diverticulum in the midesophagus. This continues to be an important mechanism for these traction diverticula but it is now believed that some may also be caused by a primary motility disorder, such as achalasia, diffuse esophageal spasm (DES), or nonspecific esophageal motility (NEM) disorder.

FIGURE 43-22 Midesophageal diverticulum.

(Adapted from Peters JH, DeMeester TR: Esophagus and diaphragmatic hernia. In Schwartz SI, J Fischer JE, Spencer FC, et al [eds]: Principles of surgery, ed 7, New York, 1998, McGraw-Hill, p 1130.)

Symptoms and Diagnosis

Most patients with a midesophageal diverticulum are asymptomatic. They are often incidentally found during a workup for some other complaint. Dysphagia, chest pain, and regurgitation can be present and are usually indicative of an underlying primary motility disorder. Patients presenting with a chronic cough are under suspicion for development of a bronchoesophageal fistula. Rarely, hemoptysis can be a presenting symptom, indicating infectious erosion of lymph nodes into major vasculature and the bronchial tree. In this case, the diverticulum is an incidental finding of lesser importance.

The diagnosis of the anatomic structure, as well as the size and location of an esophageal diverticulum, is made through barium esophagraphy. Lateral views are needed to determine from which side of the esophagus the diverticulum is protruding. Midesophageal diverticula typically present on the right because of the overabundance of structures in the midthoracic region of the left chest. It is also helpful to make a diagnosis of a concomitant fistula. A computed tomography (CT) scan is helpful to identify any mediastinal lymphadenopathy and may help lateralize the sac. Endoscopy is important to rule out mucosal abnormalities, including cancer, that may be inconspicuously hidden in the sac. In addition, endoscopy aids in identifying a fistula. Manometric studies are undertaken in all patients, symptomatic or not, to identify a primary motor disorder. Patients presenting with dysphagia, chest pain, or regurgitation in particular are manometrically evaluated. Treatment is guided by the results of the manometric findings.

Treatment

Determining the cause for midesophageal diverticula is critical for guiding treatment. In asymptomatic patients who have inflamed mediastinal lymph nodes from tuberculosis or histoplasmosis, medical treatment with antituberculin or antifungal agents is indicated. If the diverticulum is smaller than 2 cm, it can be observed. If patients progress to become symptomatic or if the diverticulum is 2 cm or larger, surgical intervention is indicated. Usually, midesophageal diverticula have a wide mouth and rest close to the spine. Therefore, a diverticulopexy can be performed where the diverticulum is suspended from the thoracic vertebral fascia. In patients with severe chest pain or dysphagia and a documented motor abnormality, a long esophagomyotomy is also indicated.

Epiphrenic Diverticula

Epiphrenic diverticula are found adjacent to the diaphragm in the distal third of the esophagus, within 10 cm of the GEJ. They are most often related to thickened distal esophageal musculature or increased intraluminal pressure. They are pulsion, or false, diverticula that are often associated with DES, achalasia and, most commonly, NEM disorders. In patients in whom a motility abnormality cannot be identified, a congenital (Ehlers-Danlos syndrome) or traumatic cause is considered. As with midesophageal diverticula, epiphrenic diverticula are more common on the right side and tend to be wide-mouthed.

Symptoms and Diagnosis

Most patients with epiphrenic diverticula present asymptomatically. They may present with dysphagia or chest pain, which is indicative of a motility disturbance. The diagnosis is often made during the workup for a motility disorder and the diverticulum is found incidentally. Other symptoms, such as regurgitation, epigastric pain, anorexia, weight loss, chronic cough, and halitosis, are indicative of an advanced motility abnormality resulting in a sizable epiphrenic diverticulum.

A barium esophagram is the best diagnostic tool to detect the presence of an epiphrenic diverticulum (Fig. 43-23). The size, position, and proximity of the diverticulum to the diaphragm can all be clearly delineated. The underlying motility disorder is often identified as well; however, manometric studies need to be undertaken to evaluate the overall motility of the esophageal body and LES. An endoscopy is performed to evaluate for mucosal lesions, including esophagitis, Barrett’s esophagus, and cancer.

FIGURE 43-23 Barium swallow showing mid and distal esophageal diverticula.

(Adapted from Pearson FG, Cooper JD, Deslauriers J, et al: Esophageal surgery, ed 2, New York, 2002, Churchill Livingstone, p 508.)

Treatment

The treatment of an epiphrenic diverticulum is similar to that of a midesophageal diverticulum. These types of diverticula also have a wide mouth and rest close to the spine. Small (<2 cm) diverticula can be suspended from the vertebral fascia and need not be excised. In patients with severe chest pain, dysphagia, or a documented motor abnormality, a long esophagomyotomy is indicated. If a diverticulopexy is performed, the myotomy is begun at the neck of the diverticulum and extended onto the LES. If a diverticulectomy is pursued, a vertical stapling device is placed across the neck and the diverticulum is excised. The muscle is closed over the excision site and a long myotomy is performed on the opposite esophageal wall, extending from the level of the diverticulum onto the LES. If a large hiatal hernia is also present, the diverticulum is excised, a myotomy performed, and the hiatal hernia repaired. Failure to repair the hernia results in a high incidence of postoperative reflux.

Motor Disorders

Motility disorders of the esophagus run on a continuum from hypomotile to hypermotile dysfunction, with intermediate types in between. There are primary and secondary motor disorders of the esophagus. Most esophageal motility disorders fall into one of five primary motor disorders: achalasia, DES, nutcracker esophagus, hypertensive LES, and ineffective esophageal motility (IEM; Table 43-2). The use of esophageal manometry has demonstrated a number of nonspecific abnormalities reflecting a spectrum of various stages of destruction of esophageal motor function that do not fit into a specific classification. Secondary motor disorders of the esophagus result from progression of other diseases, such as collagen vascular and neuromuscular diseases, and result in NEM disorders. Although the underlying pathologies are different, the presenting symptoms of primary and secondary motility disorders may be similar. A careful assessment must be done to ensure an accurate diagnosis and appropriate treatment plan.

Table 43-2 Manometric Features of Primary and Nonspecific Esophageal Motility Disorders

Achalasia

The literal meaning of the term achalasia is “failure to relax,” which is said of any sphincter that remains in a constant state of tone with periods of relaxation. It is the best understood of all esophageal motility disorders. The incidence is 6/100,000 persons/year and is seen in young women and middle-aged men and women alike. Its pathogenesis is presumed to be idiopathic or infectious neurogenic degeneration.⁵ Severe emotional stress, trauma, drastic weight reduction, and Chagas’ disease (parasitic infection with Trypanosoma cruzi) have also been implicated. Regardless of the cause, the muscle of the esophagus and LES are affected. Prevailing theories support the model that the destruction of the nerves to the LES is the primary pathology and that degeneration of the neuromuscular function of the body of the esophagus is secondary. This degeneration results in hypertension of the LES and failure of the LES to relax on pharyngeal swallowing, as well as pressurization of the esophagus, esophageal dilation, and resultant loss of progressive peristalsis.

Vigorous achalasia is seen in a subset of patients presenting with dysphagia. In these patients, the LES is hypertensive and fails to relax, as seen in achalasia. Furthermore, the contractions of the esophageal body continue to be simultaneous and nonperistaltic. However, the amplitude of the contractions in response to swallowing is normal or high, which is inconsistent with classic achalasia. It is postulated that patients in the early development of achalasia may not have abnormalities in the esophageal body that are seen in later stages of the disease. Patients presenting with vigorous achalasia may be in this early phase and will go on to develop abnormal esophageal body contractions.

Achalasia is also known to be a premalignant condition of the esophagus. Over a 20-year period, a patient will have up to an 8% chance of developing carcinoma. Squamous cell carcinoma is the most common type identified and is thought to be the result of long-standing air-fluid levels in the body of the esophagus, causing mucosal irritation and inducing metaplasia. Adenocarcinoma tends to appear in the middle third of the esophagus, below the air-fluid level where the mucosal irritation is the greatest. No specific surveillance program has yet to be initiated in patients with treated achalasia.

Symptoms and Diagnosis

The classic triad of presenting symptoms consists of dysphagia, regurgitation, and weight loss. However, heartburn, postprandial choking, and nocturnal coughing are commonly seen. The dysphagia that patients experience begins with liquids and progresses to solids. Most patients describe eating as a laborious process during which they must pay special attention to the process. They eat slowly and use large volumes of water to help wash the food down into the stomach. As the water builds up pressure, retrosternal chest pain is experienced and can be severe until the LES opens, which provides quick relief. Regurgitation of undigested, foul-smelling foods is common and, with progressive disease, aspiration can become life-threatening. Pneumonia, lung abscess, and bronchiectasis often result from long-standing achalasia. The dysphagia progresses slowly over years and patients adapt their lifestyle to accommodate the inconveniences that accompany this disease. Patients often do not seek medical attention until their symptoms are advanced and will present with marked distention of the esophagus.

The diagnosis of achalasia is usually made from an esophagram and a motility study. The findings may vary, depending on the advanced nature of the disease. The esophagram will show a dilated esophagus with a distal narrowing referred to as the classic bird’s beak appearance of the barium-filled esophagus (Fig. 43-24). Sphincter spasm and delayed emptying through the LES, as well as dilation of the esophageal body, are observed. A lack of peristaltic waves in the body and failure of relaxation of the LES are noted. Lack of a gastric air bubble is a common finding on the upright portion of the esophagram and is a result of the tight LES not allowing air to pass easily into the stomach. In the more advanced stage of disease, massive esophageal dilation, tortuosity, and a sigmoidal esophagus (megaesophagus) are seen (Fig. 43-25).

FIGURE 43-24 Barium swallow showing achalasia.

(Adapted from Dalton CB: Esophageal motility disorders. In Pearson FG, Cooper JD, Deslauriers J, et al [eds]: Esophageal surgery, ed 2 New York, 2002, Churchill Livingstone, p 519.)

FIGURE 43-25 Barium swallow showing megaesophagus.

(From Orringer MB: Disorders of esophageal motility. In Sabiston DC [ed]: Textbook of Surgery, ed 15, Philadelphia, 1997, WB Saunders, p 719.)

Manometry is the gold standard test for diagnosis and will help eliminate other potential esophageal motility disorders. In typical achalasia, the manometry tracings show five classic findings, two abnormalities of the LES and three of the esophageal body. The LES will be hypertensive, with pressures usually higher than 35 mm Hg but, more importantly, will fail to relax with deglutition (Fig. 43-26). The body of the esophagus will have a pressure above baseline (pressurization of the esophagus) from incomplete air evacuation, simultaneous mirrored contractions with no evidence of progressive peristalsis, and low-amplitude waveforms indicating a lack of muscular tone (Fig. 43-27). These five findings provide a diagnosis of achalasia. An endoscopy is performed to evaluate the mucosa for evidence of esophagitis or cancer. It otherwise contributes little to the diagnosis of achalasia.

FIGURE 43-26 Motility of the lower esophageal sphincter in a patient with achalasia.

(Adapted from Pearson FG, Cooper JD, Deslauriers J, et al: Esophageal surgery, ed 2, New York, 2002, Churchill Livingstone, p 520.)

FIGURE 43-27 Esophageal motility in a patient with achalasia.

(From Bremner CG, DeMeester TR, Bremner RM, Mason RJ: Esophageal motility testing made easy, St Louis, 2001, Quality Medical Publishing, p 75.)

Treatment

There are surgical and nonsurgical treatment options for patients with achalasia; all are directed toward relieving the obstruction caused by the LES. Because none of them addresses the issue of decreased motility in the esophageal body, they are all palliative treatments. Nonsurgical treatment options include medications and endoscopic interventions but usually are only a short-term solution to a lifelong problem. In the early stage of the disease, medical treatment with sublingual nitroglycerin, nitrates, or calcium channel blockers may offer hours of relief of chest pressure before or after a meal.⁶ Bougie dilation up to 54 Fr may offer several months of relief but requires repeated dilations to be sustainable. Injections of botulinum toxin (Botox) directly into the LES blocks acetylcholine release, preventing smooth muscle contraction, and effectively relaxes the LES. With repeated treatments, Botox may offer symptomatic relief for years, but symptoms recur more than 50% of the time within 6 months. Dilation with a Gruntzig-type (volume-limited, pressure control) balloon is effective in 60% of patients and has a risk for perforation less than 4%; however, perforation is life-threatening and must be weighed carefully in otherwise unhealthy patients.

Surgical esophagomyotomy offers superior results and is less traumatic than balloon dilation.⁷ The current technique is a modification of the Heller myotomy that was described originally by a laparotomy in 1913.⁸ Various changes have been made to the originally described procedure but the modified laparoscopic Heller myotomy is now the operation of choice. It is done open or with video or robotic assistance. The decision to perform an antireflux procedure remains controversial. Most patients who have undergone a myotomy will experience some symptoms of reflux. The addition of a partial antireflux procedure, such as a Toupet or Dor fundoplication, will restore a barrier to reflux and decrease postoperative symptoms. This is especially true in patients whose esophageal clearance is greatly impaired.⁹

Esophagectomy is considered in any symptomatic patient with tortuous esophagus (megaesophagus), sigmoid esophagus, failure of more than one myotomy, or an undilatable reflux stricture. Fewer than 60% of patients undergoing repeat myotomy benefit from surgery, and fundoplication for treatment of reflux strictures has even more dismal results. In addition to definitively treating the end-stage achalasia, esophageal resection also eliminates the risk for carcinoma. A transhiatal esophagectomy with¹⁰ or without preservation of the vagus nerve offers a good long-term result.

Results

Results of medical, interventional, and surgical procedures all point to surgery as the safest and most effective treatment of achalasia. When comparing balloon dilation to Botox injections, remission of symptoms occurred in 89% versus 38% of patients at 1 year, respectively. Studies done to compare balloon dilation versus surgery have shown perforation rates of 4% and 1% and mortality rates of 0.5% and 0.2%, respectively. Results were considered excellent in 60% of patients undergoing balloon dilation and in 85% of those undergoing surgery. Studies of laparoscopic versus open myotomy have all demonstrated superior results with a minimally invasive technique. Shorter length of stay, less pain, and excellent relief of dysphagia with an improved heartburn score have all been documented with a laparoscopic approach. Furthermore, laparoscopic myotomy appears to be safe and effective, even after treatment with Botox or balloon dilation or with a massively dilated esophagus. Although most patients present fairly early in their disease process, end-stage achalasia is still found in a small percentage of patients. In these late presentations, a surgical myotomy is not likely to be effective.

Diffuse Esophageal Spasm

DES is a poorly understood hypermotility disorder of the esophagus. Although it presents in a similar fashion to achalasia, it is five times less common. It is seen most often in women and is often found in patients with multiple complaints. The cause of the neuromuscular physiology is unclear. The basic pathology is related to a motor abnormality of the esophageal body that is most notable in the lower two thirds of the esophagus. Muscular hypertrophy and degeneration of the branches of the vagus nerve in the esophagus have been observed. As a result, the esophageal contractions are repetitive, simultaneous, and of high amplitude.

Symptoms and Diagnosis

The clinical presentation of DES is typically that of chest pain and dysphagia. These symptoms may be related to eating or exertion and may mimic those of angina. Patients will complain of a squeezing pressure in the chest that may radiate to the jaw, arms, and upper back. The symptoms are often pronounced during times of heightened emotional stress. Regurgitation of esophageal contents and saliva is common, but acid reflux is not. However, acid reflux can aggravate the symptoms, as can cold liquids. Other functional gastrointestinal complaints, such as irritable bowel syndrome and pyloric spasm, may accompany DES, whereas other gastrointestinal problems, such as gallstones, peptic ulcer disease, and pancreatitis, all trigger DES.

The diagnosis of DES is made by esophagraphy and manometric studies. The classic picture of the corkscrew esophagus or pseudodiverticulosis on an esophagram is caused by the presence of tertiary contractions and indicates advanced disease (Fig. 43-28). A distal bird beak narrowing of the esophagus and normal peristalsis can also be noted. The classic manometry findings in DES are simultaneous multipeaked contractions of high amplitude (>120 mm Hg) or long duration (>2.5 seconds; Fig. 43-29). These erratic contractions occur after more than 10% of wet swallows. Because of the spontaneous contractions and intermittent normal peristalsis, standard manometry may not be enough to identify DES. An ambulatory motility record has been identified as being able to diagnose this disease with a sensitivity of 90% and a specificity of 100% based on an identified set of abnormalities. Correlation of subjective complaints with evidence of spasm (induced by a vagomimetic drug, bethanechol) on manometric tracings is also convincing evidence of this capricious disease.

FIGURE 43-28 Barium esophagram of diffuse esophageal spasm.

(Adapted from Peters JH, DeMeester TR: Esophagus and diaphragmatic hernia. In Schwartz SI, J Fischer JE, Spencer FC, et al [eds]: Principles of surgery, ed 7, New York, 1998, McGraw-Hill, p 1129.)

FIGURE 43-29 Manometry findings in diffuse esophageal spasm.

(From Bremner CG, DeMeester TR, Bremner RM, Mason RJ: Esophageal motility testing made easy, St Louis, 2001, Quality Medical Publishing, p 83.)

Treatment

The treatment for DES is far from ideal. Today the mainstay of treatment for DES is nonsurgical, and pharmacologic or endoscopic intervention is preferred. Surgery is reserved for patients with recurrent incapacitating episodes of dysphagia and chest pain who do not respond to medical treatment. All patients are evaluated for psychiatric conditions, including depression, psychosomatic complaints, and anxiety. Control of these disorders and reassurance of the esophageal nature of the chest pain that they are experiencing is often therapeutic in and of itself. If dysphagia is a component of a patient’s symptoms, steps must be taken to eliminate trigger foods or drinks from the diet. Similarly, if reflux is a component, acid suppression medications are helpful. Nitrates, calcium channel blockers, sedatives, and anticholinergics may be effective in some cases, but the relative efficacy of these medicines is not known. Peppermint may also provide temporary symptomatic relief.¹¹ Bougie dilation of the esophagus up to 50 or 60 Fr provides relief for severe dysphagia and is 70% to 80% effective. Botulinum toxin injections have also been tried with some success, but the results are not sustainable.

Surgery is indicated for patients with incapacitating chest pain or dysphagia who have failed medical and endoscopic therapy, or in the presence of a pulsion diverticulum of the thoracic esophagus. A long esophagomyotomy is performed through a left thoracotomy or a left video-assisted technique. Esophageal manometry is a useful guide to determine the extent of the myotomy. Some surgeons advocate extending the myotomy up into the thoracic inlet, but most agree that the proximal extent generally should be high enough to encompass the entire length of the abnormal motility, as determined by manometric measurements. The distal extent of the myotomy is extended down onto the LES, but the need to include the stomach is not agreed on uniformly. A Dor fundoplication is recommended to prevent healing of the myotomy site and provide reflux protection. Results of the long esophagomyotomy for DES are variable but it can provide relief of symptoms up to 80% of the time.

Nutcracker Esophagus

Recognized in the late 1970s as a distinct entity, nutcracker esophagus is a hypermotility disorder also known as supersqueeze esophagus. It is described as an esophagus with hypertensive peristalsis or high-amplitude peristaltic contractions. It is seen in patients of all ages, with equal gender predilection, and is the most common of all esophageal hypermotility disorders. Like DES, the pathophysiology is not well understood. It is associated with hypertrophic musculature that results in high-amplitude contractions of the esophagus and is the most painful of all esophageal motility disorders.

Symptoms and Diagnosis

Patients present in a similar fashion to patients with DES with chest pain and dysphagia. Odynophagia is also noted, but regurgitation and reflux are uncommon. An esophagram may or may not reveal any abnormalities. The gold standard of diagnosis is the subjective complaint of chest pain with simultaneous objective evidence of peristaltic esophageal contractions 2 standard deviations (SDs) above the normal values on manometric tracings. Amplitudes higher than 400 mm Hg are common (Fig. 43-30). The LES pressure is normal and relaxation occurs with each wet swallow. Ambulatory monitoring can help distinguish this disorder from DES. This is of critical importance because a subset of DES patients with dysphagia can be helped with esophagomyotomy, but surgery is of questionable value in patients with a nutcracker esophagus.

FIGURE 43-30 Manometry findings in nutcracker esophagus.

(From Bremner CG, DeMeester TR, Bremner RM, Mason RJ: Esophageal motility testing made easy, St Louis, 2001, Quality Medical Publishing, p 85.)

Treatment

The treatment of nutcracker esophagus is medical. Calcium channel blockers, nitrates, and antispasmodics may offer temporary relief during acute spasms. Bougie dilation may offer some temporary relief of severe discomfort but has no long-term benefits. Patients with nutcracker esophagus may have triggers and are counseled to avoid caffeine, cold, and hot foods.

Hypertensive LES

The condition known as hypertensive LES was first described as a separate entity by Code and colleagues.¹² It was observed in patients presenting with dysphagia, chest pain, and manometric findings of an elevated LES. However, the manometric findings are not consistent with achalasia. The LES pressure is above normal and relaxation will be incomplete but may not be consistently abnormal. The motility of the esophageal body may be hyperperistaltic or normal. The pathogenesis is not well understood, but it has been theorized that it may be a similar process to that of achalasia in evolution.

Symptoms and Diagnosis

Patients with hypertensive LES present with chest pain or dysphagia. Acid reflux and regurgitation are experienced less commonly. Diagnosis is made by manometry. An esophagram may show narrowing at the GEJ with delayed flow and abnormalities of esophageal contraction; however, these are nonspecific findings. Manometry tracings demonstrate elevated LES pressure (>26 mm Hg) and normal relaxation of the LES. About 50% of the time, peristalsis in the esophageal body is normal. In the remainder, abnormal contractions are noted to be hypertensive peristaltic or simultaneous waveforms.

Treatment

The treatment of hypertensive LES is with endoscopic and surgical intervention. Botox injections alleviate symptoms temporarily and hydrostatic balloon dilation may provide long-term symptomatic relief. Surgery is indicated for patients who fail interventional treatments and those with significant symptoms. A laparoscopic modified Heller esophagomyotomy is the operation of choice. In patients with normal esophageal motility, a partial antireflux procedure (e.g., Dor or Toupet fundoplication) is added.

Ineffective Esophageal Motility

IEM was first recognized as a separate disturbance by Castell in 2000.¹³ It is defined as a contraction abnormality of the distal esophagus and is usually associated with GERD. It may be secondary to inflammatory injury of the esophageal body because of increased exposure to gastric contents. Dampened motility of the esophageal body leads to poor acid clearance in the lower esophagus. Once altered motility is present, the condition appears to be irreversible.

Symptoms

The symptoms of IEM are mixed but patients usually present with symptoms of reflux and dysphagia. Heartburn, chest pain, and regurgitation are noted. Diagnosis is made by manometry. IEM is defined as a contraction abnormality of the distal esophagus in which the total of the number of low-amplitude contractions (<30 mm Hg) plus nontransmitted contractions exceeds 30% of wet swallows. A barium esophagram demonstrates nonspecific abnormalities of esophageal contraction but will not further distinguish IEM from other motor disorders.

Treatment

The best treatment of IEM is prevention, which is associated with effective treatment of GERD. Once altered motility occurs, it appears to be irreversible.

Nonspecific Esophageal Motor Disorders

Patients with manometric findings that do not fit into one of the five classic patterns are placed in the category of nonspecific esophageal motor disorders. These nonspecific abnormalities support the understanding that esophageal motility disorders are a spectrum of abnormalities that reflect various stages of destruction of esophageal motor function. The pathogenesis of NEM is multifaceted and has no any single isolated cause. Several collagen vascular disorders are known to cause abnormalities of esophageal motility, including scleroderma, dermatomyositis, polymyositis, and lupus erythematosus. All affect the neuromuscular esophageal architecture, resulting in poor esophageal motility.

Symptoms and Diagnosis

Patients with NEM present with chest pain and dysphagia and tend to experience more reflux symptoms and regurgitation than patients with other defined disorders. Diagnostic tests include barium esophagraphy and manometric studies. Esophagraphy is helpful to rule out disorders with defined abnormalities and identifies abnormal esophageal body contractions as well as abnormalities of the LES. Manometry is critical to determine the nature of the motor abnormalities that the patient is experiencing. The LES can be normal or hypertensive, but incomplete relaxation (residual >5 mm Hg) is noted. Contractions of the esophageal body will follow one or more of the following patterns: nontransmitted, triple-peaked, retrograde, low-amplitude (<35 mm Hg), or prolonged duration (>6 seconds). Interruption of normal peristalsis at various esophageal levels is also common. Some patients will have characteristic waveforms that can be ascribed to an underlying collagen vascular disorder. Patients with scleroderma will have low-amplitude simultaneous contractions of the esophageal body, similar to those seen with achalasia, but the LES is noted to have normal or low pressure.

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